STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF …

4

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF INFLUENZA

Yes No Intoxication. CNS involvement.

Acute onset of the disease with a fast t rise, headache, vomit. Resistant red dermographism, herpetic eruption on the lips. Patients can exactly indicate the time of the beginning of thedisease

. Children suffer from intensive headache, trashingaround in their bed and broken sleep. The pain gets moreintensive when turning the head, with sound and light irritants. From the first day there is repeated vomiting, not related to foodintake. Children at early age have clonic-tonic convulsions frequently. Positive meningeal symptoms. In CBC: eosinofiliya, neutrophilic leukocytosis, elevated ESR. The nature of thecerebrospinal fluid: turbid, purulent, thousandth pleocytosis, neutrophilic character. Protein + + +. Low sugar and chloridelevels.

Men

ingo

cocc

al

men

ingi

tis

Fever syndrome, catarrh of the upper respiratory tract: profuse muco-purulent nasal discharge, mild hyperemia of posterior pharyngeal wall. Specific eye disease — purulent conjunctivitis. There is a hyperplasia of oropharyngeal lymphoid formations and lymphadenopathy of the neck. Normal CBC.

Ade

novi

ral

infe

ctio

n

Acute onset with moderate symptoms of intoxication. Catarrhal phenomena occur from the first day of illness. There is a hard, rough, dry cough, sore throat, runny nose, nasal congestion. There is a nasal discharge initially slimy,

then muco-purulent. There is swelling and redness of themucous membrane arches, soft palate, posterior pharyngealwall. Often the first manifestation of the disease is «grits»syndrome, usually at night the child suddenly wakes up from a rough barking cough. Hoarseness, noisy breathing quicklyjoin, laryngeal stenosis develops. Stenosis severity rarelyreaches 2nd degree. P

arai

nflu

enza

The presence of purulent center (otitis, sinusitis, pneumonia) often precedes development of the disease. Sudden onset, anxiety, acute headache, hyperesthesia, repeated vomiting. Early meningealsymptoms. In young children — bulging of fontanelle, separationof sutures, increased sizes of the skull. The limb paresis, staticlocomotor ataxia, cranial nerve disfunction appear. Patients arepale and cyanotic, with intensive dyspnea. Hepatosplenomegaly.Frequent development of edema — brain edema, which may causedeath in the first 3 days of the illness. In CBC: leukocytosis, with a sharp shift of neutrophils, high ESR. Cerebrospinal fluid analysis:turbid, purulent, greenish-gray fluid, neutrophil cell count —thousandths, a significant increase of protein level. Bacteriological test of CSF reveals diplococci of lanceolate form locatedextracellularly.

Pne

umoc

occa

l men

ingi

tis

Expressed catarrhal period: purulent discharge from the nose, conjunctivitis. Dry, haunting cough. Appearance of Koplik spots. Three-stage rash: 1) maculopapular

rash; 2) period of pigmentation; 3) brannyolesquamation. Leukopenia in CBC.

Mea

sles

Symptoms of nervous system impairment usually follow the inflammation of salivary glands, but both disorders can also occur simultaneously. Acute development of the disease with chill, headache, vomiting, weakness and myalgia. Meningeal symptoms are expressed moderately. Clear cerebrospinal fluid flows under high pressure, normal or slightly increased proteinlevels,

lymphocyte cell count hundredths. Сhloride and sugar

concentrations are not changed. Lumbar puncture makes patientfeel better. P

arot

itic

m

enin

giti

s S

erou

s m

enin

giti

s of

en

tero

vira

l eti

olo g

y

The main symptoms are: prolonged fever, headache, specific intoxication — stupor, hallucinations, delirium, loss of consciousness, pale and dry skin. There is a roseolous rash on the skin of the anteriorabdominal wall.

Tongue is covered with thick brown inthe center, the edges are clean, red. There are imprintsof the teeth. Diarrheal syndrome: «pea soup» feces upto 8–10 times a day. No nausea or vomiting. Hepatosplenomegaly. Positive Widal reaction.

Typ

hoid

The syndrome of «small disease» (short-term fever, nasopharyngitis) precedes the development of meningitis. Then the «big disease» occurs with the second wave of fever, headache, sweating, vomiting, impaired consciousness, tonic-clonic convulsions. Palpatory tenderness and tension of peripheral nerves. The paralysis develops on the 4–6th day of the illness. The most common spinal form — flaccid paralysis of limbs, usually legs, is found. No loss of sensitivity occurs. Liquor is transparent, colorless, pressurized. Cytosis of lymphocytic character counts hundredths. Normal protein levels.

Acute disease onset with high fever, chills, dizziness, weakness, fatigue, muscle and joint pain. There is pain in the temples, forehead, brow, eye area. There are delusions, hallucinations, nausea, vomiting related to food intake, medication, water. Light catarrhal conditions of the upper respiratory tract. Granulosity of

posterior pharyngeal wall. X-ray pattern of segmental pulmonary edema. No clinical signs of edema. In severe cases there are convulsions, transient loss of consciousness, stiff neck. It isimportant to take into account the epidemiological situation. Diagnostic testing: leukopenia with lymphocytosis, liquor withoutT T T T T T

pathological changes T T— the meningism syndromeT.

TInfl

uenz

a

Diagnostic algorithm: Seasonal influenza (Flu)

Affected

organs

Signs and

symptoms

Main

syndromes

Differential

diagnosis

Diagnosic

testing

Treatment

Specific

prophylaxis

Flu

nasopharynxlarynx and

trachealungs

central nervous system

autonomic nervous system (ANS) and

cardiovascular system (CVS)

phar

ynge

al e

ryth

ema,

rhi

niti

s

chan

ged

voic

e, r

ough

cou

gh, n

oisy

br

eath

ing,

ret

ract

ion

of c

ompl

iant

are

as

of th

e ch

est

dry

rale

s, c

yano

sis

high

fev

er, v

omit

ing,

hea

dach

e, m

uscl

epa

in, l

oss

of c

onsc

ious

ness

, con

vuls

ions

,m

enin

gism

, wea

knes

s

faci

al h

yper

emia

, abd

omin

al p

ain,

feca

l re

tent

ion,

nas

al b

leed

ing,

hem

orrh

agic

ra

sh

catarrh of the upper

respiratory tract

croupsegmental lung

impairment

encephalitic reaction,hypertensive

meningeal syndrome

abdominal pain syndrome,

hemorrhagic syndrome

aden

ovir

al in

fect

ion,

pro

drom

e of

mea

sles

, par

ainf

luen

za

diph

ther

itic

cro

up, f

orei

gn b

ody,

cro

up b

y A

RV

I

crou

pous

pne

umon

ia

toxi

c dy

sent

ery,

men

ingo

cocc

al in

fect

ion,

men

ingo

cocc

al

ence

phal

itis

, typ

hoid

, par

otit

ic m

enin

giti

s, m

enin

giti

s of

vir

al

etio

logy

appe

ndic

itis

, mes

ente

ric

aden

itis

otitis, tonsillitis, sinusitis, croup, focal and segmental pneumonia, meningoencephalitis

discharge of viruses

IFA (immunofluorescent assay) serology

neuroplegicaldesensitizing symptomaticantibioticsrehydratationdesintoxicativ

eetiotropic antifever physiotherapy vitamins restorative

vaccine interferon

5

6

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF PARAINFLUENZA

Удалено: <sp>

Diagnostic algorithm: Paraflu

Main

syndromes

Signs and

symptoms

Differential

diagnosis

Diagnostic

criteria

Complications

Treatment

Prevention

Paraflu

catarrh of the upper respiratory tract

croup asthmatic bronchitis

slight cough, slight nasal discharge, mild

hyperemia of the fauces

sudden disease onset, barking cough, changed voice , stenosis, rapid

elimination of stenosis

cough, inspiratory dyspnea, in the lungs: hard breathing and

mixed rales

measles, influenza, adenoviral infection,

RS-infection, rhinovirus infection,

meningococcal nasopharyngitis,

enteroviral infection

foreign body, diphtheria of larynx

pertussis, attack of bronchial asthma

slight intoxicationslight catarrhal

phenomenavirus isolation IFA positive results

serology: antibodies titer increased 4

times

pneumonia otitis sinusitis croup tonsillitis

desensitizing, symptomatic, revulsive, inhalation, antispasmodic meansneuroplegical, antibiotics for complications

isolation of the patient, epidemiological actions in the spot, interferon

7

8

STEPDIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF ADENOVIRUS INFECTION

Intoxication. Catarrhal syndrome.

Gradual onset of the disease with subfeb-rile temperature. Clinical signs of croup: a rough barking cough, hoarseness, noisy breathing, stenosis of the larynx. Sore throat, rhinitis, stuffy nose. Swelling and hyperemia of the mucous oropharynx.

Yes No

Par

agri

ppe

On the 4–5 days of illness maculopapular rash appears. The first elements of the rash appear as small pink spots behind the ears and on the bridge of the nose. By the end of the first days, rash covers the entire face, neck, chest, upper back. Staging of the rash is typical. Catarrhal symptoms disappear. Face is puffy, eyelids are thickened. The eyes are red, there is pus. There are abundant rashes everywhere on the skin. The disease is called «infectious rhinitis».

Stuffiness of the nose, shortness of breath and profuse nasal watery discharge. Headache in the nasal bridge, and aches all over thebody. Herpetic eruptions on the lips and on the eve of the nose. Face is slightly pasty, excessive lacrimaion, the sclera are injected. Discomfort in the throat and a little dry cough.

Rh

inov

iru

s in

fect

ion

Increase of body temperature to 38,5–39o

C, catarrh of the upper respiratory tract. Hoarse voice, dry cough, haunting, disturbing the child. Evident bilateral conjunctivitis with bright hyperemia, conjunctival edema and discharge. Koplik spots. Enanthema in the form of small pinkish-red spots on the soft and hard palate, 1–2 days before rash.

Mea

sles

, p

erio

d o

f er

up

tion

Mea

sles

, ca

tarr

hal

per

iod

Gradual onset of the disease with a rise of temperature to subfebrile level, rhinitis, loss of appetite, dry cough. There is a pale face, conjunctival hyperemia occasionally, injection of sclera vessels. There may be headache, dizziness, chills, insomnia, sweating, pain in the eyeballs, and sometimes abdominal pain, nausea, vomiting, hepatomegaly, lymphadenopathy. In the oropharynx: pharyngitis. Symptoms of bronchitis and croup are present.

Myc

opla

smai

nfe

ctio

n «Typhoid status» (stupor, hallucinations, delusions). Symptoms of intoxication are maximal evident. Skin is pale, dry, warm, face is puffy. There is a roseolous rash on the skin of stomach, sometimes on the chest and shoulders. Icteric stained of the skin of palms and feet (Filippovich symptom) is typical. There is a Padalka symptom, hepatosplenomegaly. In CBC: leukopenia, neutropenia, aneozinofiliya, lymphocytosis, elevated erythrocyte sedimentation rate.

Typ

hoid

fev

er

Punctate macular rash covers the entire surface of the skin. There are mild catarrhal symptoms. There is a lymphadenopathy. In the blood: leukopenia, lymphocytosis, plasma cells. There is a peripheral lymph nodes enlargement, especially the occipital and back cervical. The rash is localized on extensor surfaces of the limbs around the joints, on the back and buttocks. After the elimination of the rash there is no signs of pigmentation or desquamation.

Ru

bel

la

The main signs of the disease are mild sore throat, slight dry cough, runny nose (sometimes), hyperemia of the pharynx, enanthema. Then the bubbles → erosion→ epithelization appear. By the end of the week enanthema and other manifestations of the disease completely disappear. There is a short duration of the course.

Her

pan

gin

a

Acute onset with body t over 38 C, whichpersists

o

for a long time (sometimes up to 10 days or more). Conjunctivitis, lymphadenopathy. First, the defeat of one eye, then the second. Cough is wet, mild hyperemia of the pharynx and pharyngitis. There is hepatosplenomegaly. In CBC - moderate leukocytosis with neutrophilia, lymphopenia, slightly increased ESR.

Ad

enov

iral

in

fect

ion

There is a swelling of bronchial mucosa, obstruction, bronchospasm. Cough is dry at first, then it becomes wet with discharge of mucus. Moist, dry rales are auscultated (medium, rarely fine bubbling rales). Longer process of exhalation, difficulty of breath.

Bro

nch

itis

Diagnostic algorithm: Adenoviral infection

Clinical forms

and syndromes

Signs and symptoms

Differential

diagnosis

Complications

Diagnosis

Treatment

Epidemiological

characteristics

adenoviral infection

URTCpharyngoconjctunival

fever intersticial syndromesyndrome of croup astmatical syndrome

mononucleosis-like syndrome

Long fever, membraneous conjunctivitis,

follicular conjunctivitis, catarral

conjunctivitis, pharyngitis

Liquid stool, vomiting

Rough cough, voice change, stenotical

breath

Expiratory dyspnea, noisy breath, whistlinglargely - and medium

bubbling rale

inlargementof lymph nodes

, abdominal pain, enlargement of the

liver, enlargement of the lien

fever, weakness, appetite decrease, occasional vomiting,

intensive rhinorrhea, puffy face, cough, hyperemia of the

pharynx

fluparainfluenzaRC infection

prodrome of measlesdiphtheria-eye

enteroviral infectionwith intestinal syndrome

dysenterycoliinfectionsalmonellosisappendicitis

mesenteric adenitis different etiologiesinfectious mononucleosis

sinusitisotitispneumoniatonsillitis

IFA CFT swabs

symptomatic desensitisation restorative stimulatingantibiotics for complications

source of infection pathways seasonality isolation of patientsevents in the site of

infection

9

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF MYCOPLASMA INFECTION

Catarrhal symptoms. Intoxication.

Respiratory distress syndrome.

No Yes

Gradual onset of the disease with subfebrile fever. The main clinical signs are rhinitis, loss of appetite, dry cough, intoxication, pallor, conjunctival hyperemia, vascular injection of the sclera, pain in eyeballs. There is an abdominal pain, nausea, vomiting, hepatomegaly, lymphadenopathy. Symptoms of intoxication are little evident. Pharyngitis, catarrhal conditions, the symptoms of bronchitis and of croup (sometimes) develop. In the lungs there is a rough breath, inconstant scaffered rales. In CBC: moderate leukocytosis, neutrocytosis, increased ESR. M

ycop

lasm

a in

fect

ion

Bronchiolitis and bronchitis with severe bronchial obstruction are typical. There is a catarrhal syndrome, hyperemia of the fauces, subfebrile or normal temperature. There is a mild headache, chilling, chest pain, dry cough, expiratory dyspnea, perioral

infe

ctio

n

cyanosis.

RS

-

Percussion: vesiculotympanitic sound. Auscultation: crepitus fine bubbling rales.

Evident catarrhal phenomena accompanying with large nasal discharge, hyperplasia of lymphoid structures of the stomatopharynx, conjunctivitis, swollen lymph nodes, lack of changes in the peripheral blood (normal CBC). There is a wet cough, throat congestion, intoxication, possible muscle and joint pain. In young children the diarrhea of

Ad

enov

iral

in

fect

ion

enteritis character is possible.

The disease develops after contact with birds (pigeons, poultry). Acute onset with high fever and marked toxemia in the absence of catarrhal symptoms or upper respiratory tract pathology. The possibility of relapse and late myocarditis, hepatosplenomegaly, leukopenia, increased ESR, a longer course of disease. In addition, pneumonia signs can develop.

Orn

ith

osis

Acute onset with high fever, intoxication, flushing, injection of sclera vessels, puffy face, hyperemia of the tonsils and soft palate. Tracheitis, tracheobronchitis and focal pneumonia develop. There are pains in the eyeballs, muscle pain, abdominal pain, bowel disorders. Hallucinations, hepatosplenomegaly, prolonged fever, headache, insomnia and mental instability are possible. In severe

Q f

ever

cases: serous meningitis and encephalitis.

The disease proceeds with toxicosis. The onset is percute with coughing up blood, shortness of breath, sharp chest pain. The diaphragmatic pleura gets involved in the process, with pain radiating to the abdomen. There is an impaired consciousness, delirious state. Neutrophilic leukocytosis and high ESR are typical changes in CBC. Prescription of antibiotics results in rapid improvement.

Cro

up

ous

pn

eum

onia

10

Diagnostic Algorithm: mycoplasma infection

Etiology

Mechanism

of transmission

Affected organs

and tissues

Signs and

symptoms

Clinical course

Diagnostic

tests

Differential

diagnosis

Treatment

Prevention

mycoplasma infection

mycoplasmas

aerborne

broncho-pulmonary system -

nasopharyngitis, pharyngitis,

laryngitis, bronchitis,pneumonia

eye - eye damage, pain of the eyeballs

(vascular membrane)joints - arthritis liver - hepatitis

central nervous system - meningitis

kidney - nephritis, abacterial urethritis

sw

elli

ng, t

ende

rnes

s, li

mit

atio

n of

mov

emen

t

into

xica

tion

, rai

sing

the

tem

pera

ture

to f

ebri

le le

vel,

head

ache

, sor

e th

roat

, hy

pere

mia

of

the

thro

at, d

iffi

cult

y in

nas

al b

reat

hing

. Fro

m 4

-5 d

ays

scan

ty

expe

ctor

atio

n. T

here

are

som

etim

es th

e sy

mpt

oms

of c

roup

. In

the

lung

s, th

ere

is a

ha

rd b

reat

hing

, inc

onst

ant s

catt

ered

dry

ral

es. I

n pn

eum

onia

ther

e ar

e c

hest

pai

ns

pai

n in

the

eyeb

alls

, hyp

erem

ia o

f th

e co

njun

ctiv

a, i

njec

tion

ves

sels

of

scle

ra,

dam

age

to th

e ch

oroi

d

hep

atom

egal

y

hea

dach

es, m

enin

geal

sym

ptom

s

freq

uent

uri

nati

on w

ith

smal

l por

tion

s, th

e sy

mpt

oms

of n

ephr

itis

intr

aute

rine

fet

al le

sion

mis

carr

iage

, pre

mat

urit

y, g

ener

aliz

ed f

orm

of

dam

age a

nd

cent

ral n

ervo

us s

yste

m d

amag

eacute

Bacteriological: isolation of mycoplasma from pharyngeal

mucus, pus, sputum

complement fixation test and reaction of indirect

hemagglutination, latex - agglutination, diffusion in the

gel

ARVI (adenoviral, RS - infection)

ornithosis Q-fever croupous pneumonia

symptomatic therapy antibioticsdisintoxicational means,

plasmadiuretics

Early isolation of patients

common preventive measures

11

39

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF ENTEROVIRAL INFECTION

Yes No Exanthema syndrome. Intoxication.

Maculo-papular rash, first behind the ears, on the bridge of the nose with tendency to merger. On the 2 daynd — on the body and hands. On the 3rd day — on the lower limbs. Staging of the rash, Koplik spots and conjunctivitis are typical.

Mea

sles

Normal or subfebrile temperature

Macular large-spotted hemorrhagic rash appears lately (on the 6–7th day of the disease). Localization - relatively uniformly covers the whole body. There is itching of the skin. After disappearance of the rash the scaling of the skin is observed, often there is defurfuration. Kidneys are affected. Hepatosplenomegaly. CBC: leukocytosis, elevated ESR level.

Lep

tosp

iros

is

Maculo-papular rash, more abundant on the face with tendency to merger. After the disappearance of the rash pigmentation and skin exfoliation may de-velop. There is no staging of the rash. At the time of rash appearance and before there is no decrease and a new increase of body temperature. Tonsillitis is typical. CBC: atypical mononuclear cells. Lympha-denopathy develops.

Large-spotted macular rash, doesn’t merge, with no staging. With underlying fever there is swelling and puffiness of face, the muscle soreness and significant eosinophilia. From medical history: consumption of not enough processed meat 1–4 weeks before the disease.

Infe

ctio

us

mon

onu

cleo

sis

Tri

chin

osis

There is a punctuate macular pinkish-red rash on the background of unchanged skin. Elements of the rash do not merge. The rash initially appears on the face, then within a few hours it spreads throughout the body. There is a localization on the extensor surfaces of the extremities, around the joints, back and buttocks. The rash lasts for 2–3 days. It disappears without pigmentation and desquamation.

Ru

bel

la

There is at the beginning a pink-red spot of oval form on the chest with a small scaling in the center («parent plaque»). Then there is macular rash on the whole body. There are oval spots up to 15 mm, with the peeling in the center, less intensive painted with bright red border on the periphery.

Pin

k li

chen

The profuse rash, roseolic and papulous, evident on the trunk, prone to merger, is present for up to –3 weeks, then gradually pales and disappears. There is a presence of residual effects of primary syphilides (hard chancre).

Syp

hil

is

Rash appears in the first days after taking the drugs. There is an itchy skin, swollen lymph nodes and mild eosinophilia. Rash merges, there is no staging.

Med

icam

enta

l d

erm

atit

is

Abundant macular rash on the extensor surfaces of limbs with concentration in the large joints, on the buttocks. There are single elements on the body, and there is no rash on the face. Hyperemia of face and neck, vascular injection of the sclera vessels, hepatosplenomegaly are typical. R

osen

ber

g in

fect

iou

s er

yth

ema

Acute onset of the disease. Macular rash with tendency to fusion, more intense on the trunk. There is no staging. After the disappearance of the rash and pigmentation, desquamation stay. Signs of serous meningitis and epidemic myalgia were found. The rash persists for 3–4 days.

En

tero

viru

s ex

anth

ema

Enteroviral infection (Boston exanthema)

DIAGNOSTIC ALGORITHMS : ENTEROVIRAL INFECTION

Clinical forms

Signs and

symptoms

Differential

diagnosis

Principles

of treatment

Diagnostic

criteria

Epidemiology

Enteroviral Infection

serous meningitis

epidemic myalgia

exanthema herpanginaPoliomyelitis-

likeviral

diarrheaencephalo

myocarditisfe

ver,

hea

dach

e, n

ause

a, v

omit

ing,

abd

omin

al

pain

, mus

cle

pain

, m

enin

geal

sym

ptom

s

hype

rem

ia o

f th

e fa

ce, h

eada

che,

exc

ruci

atin

g m

uscl

e pa

in

feve

r, h

eada

che,

mus

cle

pain

, vom

itin

g,

mac

ulop

apul

ar r

ash

feve

r, h

eada

che,

her

pes

rash

in p

hary

nx

mus

cle

pain

, cha

nge

in m

anne

r of

wal

king

, as

ymm

etry

of

tend

on r

efle

xes,

hyp

oten

sion

cata

rrha

l syn

drom

e, v

omit

ing,

sub

febr

ile

tem

pera

ture

, ent

erit

ic f

eces

anor

exia

, som

nole

nce,

dia

rrhe

a, f

ever

, gen

eral

cy

anos

is, t

achy

card

ia, c

ardi

ac a

rrhy

thm

ias,

ca

rdia

c no

ise,

hep

atol

iena

l syn

drom

e, s

tres

s of

fo

ntan

elle

, cra

mps

Par

otit

ic m

enin

giti

s, p

olio

mye

liti

c m

enin

giti

s, m

enin

goco

ccal

m

enin

giti

s, tu

berc

ulou

s m

enin

giti

s

appe

ndic

itis

, ple

uris

y, in

flue

nza

mea

sles

, sca

rlet

fev

er, r

ubel

la,

infe

ctio

us e

xant

hem

a

herp

etic

sto

mat

itis

, aph

thou

s st

omat

itis

, ac

ute

resp

irat

ory

dise

ase

mil

d fo

rms

of p

olio

mye

litis

coli

infe

ctio

n, s

taph

yloc

occa

l en

tero

coli

tis,

sal

mon

ello

sis,

sim

ple

dysp

epsi

a

seps

is, a

cute

inte

stin

al in

fect

ions

, m

enin

gitis

desensitization

vitamin therapy

disintoxication

dehydrationanalgetics, antipyretics

hormones cardiacs

polymorphism of

clinical manifestatio

ns

prolonged fever with

severe intoxication

acute onsetepidemic anamnesis

isolation of enteroviruse

sserology

Positive immunofluore

scence

seasonalitytransmissionsource focality immunity

40

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF SPINAL FORM OF POLIOMYELITIS

No Yes Syndrome of flaccid paralysis.

Liquor syndrome.

The paralyses are characterized by acute rapid development; with period of increasing intensity from a few hours to 1-2 days. Paralyses are asymmetric, even on the same limb; different muscle groups can have different degree of damage. There are no signs of sensitivity failure, pelvic or pyramidal disorders. Typical pain syndrome: spontaneous pain in the limbs and back, painful palpation of nerve trunks. The recovery period takes 1-3 years.

Pol

iom

yeli

tis

(sp

inal

for

m)

It is characterized by sparing gait.The child tries not to step on theaffected leg, bends the knee and spares it. Passive motion and palpation are painful. Tendon reflexes and tone are preserved.Normal cerebrospinal liquid normal. In CBC: marked

som

atic

O

steo

arti

cula

r p

ath

olog

y (b

urs

itis

, art

hri

tis,

low

bac

k p

ain

, et

c.)

inflammatory changes.

Central paralysis characterized by symmetry, conduction disturbancesof sensitivity, high tonus, lively reflexes, pyramidal signs, rough and chronic pelvic disorders, trophic disorders M

yeli

tis

with the bedsoresformation.

It is often characterized by fever-freeonset, with increasing, sometimes long and wavy, development of paralyses,which are symmetrical andpredominantly distal. Polineuritic and radicular type of sensitivity impairment. CSF: increased protein with normal cell count.

Pol

yrad

icu

lon

euri

tis

Fever, catarrhal signs, herpangina, myalgia syndrome, diarrhea, exan-thema. Absent or smoothed meningoencephalitic syndrome, limited character of paresis. The normal state is of the CSF. Complete recovery of paresis is in the first 2

Pol

iom

yeli

tis-

lik

e di

seas

es

ente

rovi

ral i

nfe

ctio

n)

months of the disease.

(

12

DIAGNOSTIC ALGORITHMS: POLIOMYELITIS

Type

Clinical

forms

Signs and

symptoms

13

Differential

diagnosis

Characteristics of the

modern poliomyelitis

Stages

Diagnosis

Prevention

Therapeutic

strategies

POLIOMYELITIS

Typical Atypical

Paralytic

BulbarSpinal Pontinha

Flaccid paralysis,

asymmetry ofparalysis

Aphonia, snuffles, choke,

paradoxical breathing

Paralysis of facial nerve

AsymptomaticNon paralytic Obliterated

General infection "abortive"

Meningeal

Cough, sore throat, hyperemia of the throat, abdominal

pain, bloating, abdominal tension, frequent liquid stool

Occipital muscular rigidity, positive

Kernig's and Brudzinskiy's

symptoms

High fever, weakness, lethargy, headache, vomiting, poor appetite, hypersensitivity, pain in

the extremities, sweating, thirst, tachycardia

Poliradiculo-neuritis

OsteomyelitisDiphtheria polyneuritis

MyelitisEnteroviral infection

(paralytic)

Foreign body in airways

Peripheral neuritis of the facial nerve

FluIntestinal infections

Meningitis of different etiologies

Absence of cyclicity

Normal temperature

Good quality flow

Easy spinal paralysis

ParalyticPreparalytic ReplacementResidual effects

Complement fixation test,

neutralization

Virus isolation

Dynamics of liquorologic parameters

Quarantine DisinfectionEarly

admission to h it l

Active immunization

Miobiostimulyators

Medicaments that improve

nerve conduction

Medicaments that increase

reactivity, vitamins

EXERCISE therapy,

massage, spa, physiotherapy

Mixed forms

Hormones

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF DISEASES ACCOMPANIED BY EXANTHEMA

Symptoms Scarlet fever Pseudotuberculosis

Measles Rubella Meningococcemia Chicken pox

Availability prodrome No No Yes, 3–4 days Absent or 1–2 days No Absent

Body temperature Febrile, 3–5 days Febrile, 4–6 days Subfebrile 3–4 days, then febrile 3 days

normal or subfebrile 2–3 days

Febrile, 5–7 days Subfebrile or febrile 3–5 days

Catarrh of the upper respiratory tract

Absent expressed expressed poorly expressed Absent Absent

Angina Typical (catarrhal, lacunar, necrotic)

Absent Catarrhal Absent Absent Absent

Conjunctivitis Absent typical typical hardly ever Absent Absent

Intoxication Moderately expressed, persists 3–5 days

Expressed, preserved more than

5 days

Moderate, persists 6–8 days slightly expressed or absent

severely expressed, persists 3–5 days

slightly expressed, persists 3–5 days

Time of the rash appearing On the 1–2 day The end of 1 week On the 4–5 day On the 1–2 day On the 1–2 day On the 1st day

Duration of the rise of the rash

1 day 1–3 days 3 days stage: face-trunk -limb

1–2 days 1–2 days 3–5 days, jerky

Character of rash Micropunctate rash, in concentarated places — petechial

with hyperemia

Micropunctate rash with hyperemia

Maculopapular, prone to merger

Predominantly spotted

Haemorrhagic, irregular shape, with central necrosis

«False» polymorphism: a spot-papule- vesicle- crust

The preferential localization of rash

Natural folds, the lateral surface of the trunk, flexion of the legs, lack

of nasolabial triangle

Symptom of «glove», «socks»,

«hood»

Does not have special localiza-tion places

The largest number in the buttocks, extensor surfaces of extremities

Mainly in the buttocks, legs Does not have special localization places

Pigmentation Absent Absent Present Absent Absent Absent

Desquamation Macroscaling — on the palms, soles,

scaly — on the trunk

macroscaling — on the palms, soles, scaly — on body

Scaly Absent Absent Absent

Enanthema Micropunctate rash, pink in color, in soft and hard palate, appears simultaneously with exanthema

Meets not permanently

1) on the buccal mucosa, gums, lips - whitish papules: Belsky –Filatov–Koplik, s spot, appear on 2–3 days of illness and persist for 2–3 days 2) on the mucosa of hard and soft palate - the pink spots appear simultaneously with exanthema

may be on the mucosa of the soft and hard

palate, appear simultaneously with

exanthema

Absent Erosion on the oral mucosa

The state of tongue Coated in the first 1–2 days, then the "strawberry"

Coated in the first 1–2 days then «strawberry»

without features without features Normal Normal

cardiovascular system and other organs impairment

1st week — the sympathetic phase: tachycardia, a tendency to the

increased blood pressure; 2nd week — vagus phase:

bradycardia, decreased blood pressure,

enlarged heart borders

Organ failure, depending on the

severity of the process

without features without features Frequent development of infective toxic shock, purulent meningitis

Normal

Lymphatic nodes increased submandibular lymph nodes

The increase in mesenteric lymph

nodes

without features increased occipital andback cervical lymph

nodes

Normal Normal

39

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF ENTEROVIRAL INFECTION

Yes No Exanthema syndrome. Intoxication.

Maculo-papular rash, first behind the ears, on the bridge of the nose with tendency to merger. On the 2 daynd — on the body and hands. On the 3rd day — on the lower limbs. Staging of the rash, Koplik spots and conjunctivitis are typical.

Mea

sles

Normal or subfebrile temperature

Macular large-spotted hemorrhagic rash appears lately (on the 6–7th day of the disease). Localization — relatively uniformly covers the whole body. There is itching of the skin. After disappearance of the rash the scaling of the skin is observed, often there is defurfuration. Kidneys are affected. Hepatosplenomegaly. CBC: leukocytosis, elevated ESR level.

Lep

tosp

iros

is

Maculo-papular rash, more abundant on the face with tendency to merger. After the disappearance of the rash pigmentation and skin exfoliation may de-velop. There is no staging of the rash. At the time of rash appearance and before there is no decrease and a new increase of body temperature. Tonsillitis is typical. CBC: atypical mononuclear cells. Lympha-denopathy develops.

Large-spotted macular rash, doesn’t merge, with no staging. With underlying fever there is swelling and puffiness of face, the muscle soreness and significant eosinophilia. From medical history: consumption of not enough processed meat 1–4 weeks before the disease.

Infe

ctio

us

mon

onu

cleo

sis

Tri

chin

osis

There is a punctuate macular pinkish-red rash on the background of unchanged skin. Elements of the rash do not merge. The rash initially appears on the face, then within a few hours it spreads throughout the body. There is a localization on the extensor surfaces of the extremities, around the joints, back and buttocks. The rash lasts for 2–3 days. It disappears without pigmentation and desquamation.

Ru

bel

la

There is at the beginning a pink-red spot of oval form on the chest with a small scaling in the center («parent plaque»). Then there is macular rash on the whole body. There are oval spots up to 15 mm, with the peeling in the center, less intensive painted with bright red border on the periphery.

Pin

k li

chen

The profuse rash, roseolic and papulous, evident on the trunk, prone to merger, is present for up to 2– weeks, then gradually pales and disappears. There is a presence of residual effects of primary syphilides (hard chancre).

Syp

hil

is

Rash appears in the first days after taking the drugs. There is an itchy skin, swollen lymph nodes and mild eosinophilia. Rash merges, there is no staging.

Med

icam

enta

l d

erm

atit

is

Abundant macular rash on the extensor surfaces of limbs with concentration in the large joints, on the buttocks. There are single elements on the body, and there is no rash on the face. Hyperemia of face and neck, vascular injection of the sclera vessels, hepatosplenomegaly are typical. R

osen

ber

g in

fect

iou

s er

yth

ema

Acute onset of the disease. Macular rash with tendency to fusion, more intense on the trunk. There is no staging. After the disappearance of the rash and pigmentation, desquamation stay. Signs of serous meningitis and epidemic myalgia were found. The rash persists for 3–4 days.

En

tero

viru

s ex

anth

ema

Enteroviral infection (Boston exanthema)

14

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF HERPETIC INFECTION (SIMPLE HERPES)

Удалено: <sp>

Diagnostic algorithms : herpetic infection

Etiology

Seasonality

The mechanism

of transfer

Affected organs

and systems

Clinical

forms

Flow

Diagnostic

tests

Differential

diagnosis

Principles

of treatment

Prvention

Herpetic infection

Herpes simplex virus

Winter time

Airborne transplaсentalSexual Household contact

GenitalsFacial skin and oral

mucosacentral nervous system Liver Lungs Eyes Kidneys

Affected mucous membranes

Genital herpes Pathology of central

nervous systemSkin pathology Affected eye Visceral form

Sto

mat

itis

, gin

giva

stom

atit

, rai

sing

the

tem

pera

ture

to 3

9°C

, fev

er, r

estl

essn

ess,

re

fusa

l to

eat,

incr

ease

d sa

liva

tion

, col

d so

res

on th

e bu

ccal

muc

osa,

tons

ils,

incr

ease

d re

gion

al ly

mph

nod

es

Aff

ecte

d pe

nis,

vul

va, v

agin

a, c

ervi

x, p

erin

eum

uret

hra,

end

omet

rium

Enc

epha

liti

s, m

enin

goen

ceph

alit

is, n

euri

tis

Her

peti

cal l

ip, n

ose,

eye

lids

, fac

e, h

ands

, he

rpet

ical

ecz

ema

Con

junc

tivi

tis,

ble

phar

ocon

junc

tivi

tis,

ke

rati

tis,

ker

atoi

rido

cycl

itis,

cho

rior

etin

itis

, uv

eiti

s, r

etin

al p

eriv

ascu

liti

s

Hep

atit

is, p

neum

onia

, her

peti

cal n

ephr

itis

AbortifacientAcute Recurring

Allergic testSwabs or scrapings from

infected tissuesReaction of passive

hemagglutination

Reaction of binding complement

Enzyme immunoassay Neutralization reaction of the virus

Interpretation of immunograms

Herpes zoster HIV infectionVaccination eczemaAdenoviral

keratoconjunctivitisMeningitis Chickenpox

Enterovirus infection accompanied by

herpetic eruptions

Vitamin therapy ImmunomodulatorsPainkillersAntiviralLocal

0.25% oxalic ointment, 0.5% ointment florenal,

0.2–0.5% ointment tebrofen

Hyperimmunoglobulin,normal

immunoglobulin

Vitamins of group В (В1, В2, В12)

Anestezin, lidocaine

Acyclovir adeninarabinozin, viroleks, ribovirin,

ganciclovir

Bacterial examination of the contact

Dispensary observationIsolation of patientsHardeningSanitary and hygienic

regime

15

16

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF CHICKENPOX

Vesicular rash

Yes No Fever, symptoms of intoxication

There is a herpetic rash — a group of closely spaced vesicles filled with clear contents. Mucous mem-branes, skin, eyes, genitals and nervous system are-affected. The rash is usually located around the mouth, lips, on the wings of the nose, sometimes on the face and trunk, and it is itching and burning.

Her

pes

si

mp

lex

There are bright juicy edematous erythema, serous papules, microvesicles on the cheeks, forehead, extensor surfaces of extremities agains the backround of itching, which are rapidly opens and form the typical erosion («serous wells»). When erosions merge they form large weeping areas in places covered with crusts.

Ecz

ema

There is a sudden onset of disease with extensive erythematous spots. There are huge bubbles on their background (similar to the burn of III degree). There are bubbles on the background of hyperemic skin, detachment of the epidermis. Eroded surface remains after the rupture of the bubble. There is a positive Nikolsky's symptom.

Lye

lls ’

syn

dro

me

There is a polymorphic exudative erythema, accompanied by severe damage not only of the skin, but also of mucous membranes. Localization is on the trunk, neck, face, extremities. The rash consists of spots, papules, vesicles and blisters. Evident lesions of the mouth mucous membranes, nose, conjunctiva and genitals can be found. On the palms and soles there are round dark-red spots with hemorrhagic manifestations.

At first vesicles form on the mucous membrane, then they burst quickly and convert to erosion which causes a sharp pain during swallowing. It is characterized by rhythmicity with the change of the four periods Vertigo, tinnitus and insomnia. There are symptoms of cardio-vascular weakness, seizures, loss of consciousness. There is a hepatosplenomegaly. Diuresis is reduced.

Acute onset of the disease. By the 3–4 dayth on the backdrop of a temporary reduction of body tempera-ture the rash appears. Elements of the first rash are detected on the face, hands, and then on the trunk. The cycle of development: spot–papule–vesicle –erosion–crust–scar. Less susceptibility of people to that disease . The stages of the disease change quickly.

The rash is polymorphic. Skin, mucous membranes of the mouth and genitals are affected. Typical rash changes by stages. The final element of the rash is the crust. Bubbles are unicameral. At the peak of the disease there are swollen lymph nodes, liver, spleen enlarged rarely. The body temperature is 39–40oC, there is sometimes a chill.

Ste

ven

s-Jo

hnso

ns

s

’

ynd

rom

e N

atu

ral

smal

lpox

M

onk

eyp

ox

Ch

ick

enp

ox

A lot of small bubbles the size of a millet seed, thickly arrange, especially on the chest and abdomen, on a slightly reddened skin. First, the bubbles are transparent, then dry up and grow turbid. There is a slight itch of the skin, profuse sweating

hea

t ra

sh

There is a persistent intertrigo on the skin folds, dry and pale skin, gneiss, cradle cap, the growth of abnormal body weight (pastoznost, friability). There may be erythematous-papulo-vesicular rash on the trunk and extremities. "Geographic" tongue, conjunctivitis, rhinitis, catarrh of the respiratory tract are typical. There is an exposure of the food allergens.

exu

dat

ive-

cata

rrh

al d

iath

esis

There are itch burrows on the palms and soles. There is a profuse rash in the form of blisters, spots, vesicles and soak on the face, scalp, neck, hands (mostly on the flexor surface), hips, legs, around the navel and nipples. The positive effect of rubbing 5% sulfur ointment mixed with balsam Shostakovich, 2 times a day for 5 days.

Sca

bie

s

The rash appears during the first days after taking the drugs. Itchy skin, swollen lymph nodes and mild eosinophilia. Rash blends, there is no stages. There are cutaneous lesions of the mouth, tongue, eyes, mouth, stomach and intestines mucous membranes. It can be caused by penicillins, cephalosporins, tetracyclines, sulfonamides.

Dru

g al

lerg

y

DIAGNOSTIC ALGORITHMS : VARICELLA

Affected

organs

Symptoms and

syndromes

Characteristics

of the rash

The indicators

of severity

Complications

The differential

diagnosis

Principles

of treatment

Prevention

Epidemiological

characteristics

Chicken pox

Mucosal membranes Skin Central nervous system Other

Ena

nthe

ma

Ras

h, it

chin

g

Hyp

erth

erm

ia,

inso

mni

a, h

eada

che,

an

orex

ia, v

omit

ing,

de

liri

um

Mil

d m

onoc

ytos

is,

lym

phad

enop

athy

, mil

d le

ukop

enia

, mod

erat

e ly

mph

ocyt

osis

Resh, spot, papule, vesicle, local polymorphism, the

lack of favorite localization

Plentiful rash Evident Failure of internal organs

Abs

cess

es

Phle

gmon

Ery

sipe

las

Gan

gren

e

Pneu

mon

ia

Enc

epha

liti

s

Lym

phad

enit

is

Stom

atit

is

Pyod

erm

ia

Pyodermia

Herpes sim

plex and

herpes zoster

Scabies

Strophulyus

Impetigo

Variola

Insect bites

Scarlet fever

Sym

ptom

atic

ther

apy

Toi

let o

f sk

in a

nd

muc

ous

mem

bran

es

Des

ensi

tizi

ng th

erap

y

Eti

otro

pic

trea

tmen

t of

com

plic

atio

ns

Hyg

ieni

c re

gim

en

Qua

rant

ine

for

thos

e w

ho c

onta

cted

the

pati

ent

Qua

rant

ine

for

the

pati

ent

Peri

od o

f qu

aran

tine

fo

r th

e pa

tien

t

Ear

ly d

iagn

osis

inst

able

in th

e en

viro

nmen

t

maj

or v

irus

drop

let s

prea

d

17

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSTICS OF CONGENITAL CMV INFECTION

IN CHILDREN YOUNGER THAN 1 YEAR OLD

No Yes Syndrome of intrauterine infection at fetus and newborn

The risk of abortion is high. The disease manifests at birth with jaundice, hepatosplenomegaly, hemorrhagic purpura. The color of urine gets darker and feces color becomes bright. Muscular hypotonia, hyporeflexia and convulsions occur. Microcephaly, hydrocephaly, septum and aortic valves cleft and others are often affected. Malformations of the kidneys and gastrointestinal tract are typical.

Cyt

omeg

alov

iru

s in

fect

ion

An abortion can occur as a result of congenital toxoplasmosis infection. At birth infected baby has a triad:

Tox

opla

smos

is

hydrocephalus, intracranial calcifications and chorioretinitis. Hepatosplenomegaly, jaundice, intoxication, fever, polymorphic rash, hemorrhagic syndrome, anemia, possible generalized lymphadenopathy and cataract also can occur.

Abortion is frequently possible. A baby is prematurely born, with the signs of malnutrition. In the first few days the temperature rises sharply, peripheral circulation is impaired and jaundice appears. Leading syndrome is respiratory failure (distress or pneumonia). Rashes on the skin and mucous membranes are roseolous, papular and petechial. It characterized by the appearance of grayish-white granulomas, sized of a millet grain on the swollen mucous membranes of the stomatopharynx, the back of the throat, on the tonsils. It is characterized by meningitis, meningoencephalitis.

Lis

teri

osis

Intrauterine infection may cause an abortion. When the disease affects children there is a marked intoxication, hemorrhagic syndrome and the symptoms of acute cardiovascular insufficiency develop. Jaundice, hemorrhagic syndrome, intracranial calcifications, choreoretinitis, microphthalmia and cataracts are possible complications. Skin and visible mucus damages are rare. But if it occurs, the vesicular rash appears on 5–7 days of life.

Her

pet

ic in

fect

ion

(H

erp

es s

imp

lex

viru

s)

Premature delivery is possible. Cataracts, heart defects and deafness form the typical triad. Retinopathy, microphthalmia, glaucoma, micro and hydrocephalus, cleft soft and hard palate, cryptorchidism, hypospadias, congenital hepatitis are also typical. Thrombocytopenia and hemorrhagic syndrome are ofte

Ru

bel

la

n observed.

Infection of the child occurs during the passage of mother’s birth canal. It manifests with granulation conjunctivitis and pneumonia. The disease has a torpid course. It is complicated by blepharitis, stenosis of lacrimonasal tract, scarring of the conjunctiva. Cough is dry first, then paroxysmal with a lot of mucus. Dissociation is between marked dyspnea and scant

TCh

lam

ydia

infe

ctio

n

37h i l d

DIAGNOSTIC ALGORITHMS: CYTOMEGALOVIRAL INFECTION

Etiology

The source of infection

The mechanism

of transfer

Classification

Affected

organs and systems

Clinical forms

Methods of

diagnosis

Clinical course

Treatment

Prophylaxis

CYTOMEGALOVIRAL INFECTION

kind Herpes viridae

A sick person and virus carrier

Contagious Airborne Sexual Parenteral

Ant

ivir

al: c

yclo

fero

n,

ganc

yclo

vir,

acyc

lovi

r, V

alac

yclo

vir

Ant

ibio

tics

for

bact

eria

l in

fect

ion

stra

tifi

cati

on

Cor

tico

ster

oids

—

pred

niso

lonu

m

Vit

amin

ther

apy:

vit

amin

s B

,C

, K, PPCR

Treponema pallidum

hemagglutination

Complement fixation test

Neutralization reaction

Congenital Acquired

Detection of cytomegalovirus in the

sediments of urine, saliva, cerebrospinal fluid

LiverHemopoetic

organs Lungs Intestines KidneysHeart Salivary glands

CNS

Screening of pregnant

women for CMV

Use of condoms

During blood transfusion s:

transfusions of blood and blood

components from seronegative donors

Transplacental M

icro

ceph

aly,

miс

rogi

ria,

bra

in

arch

itect

onic

s im

pair

men

t wit

h

men

tal r

etar

datio

n de

velo

pmen

t

Atr

ial a

nd v

entr

icul

ar s

epta

l cl

eft,

end

ocar

dium

fi

broe

last

osis

, mal

form

atio

ns o

f th

e ao

rtic

val

ve a

nd p

ulm

onar

y tr

unk

Hep

atom

egal

y, ja

undi

ce

(liv

er a

cts

unde

r th

e co

stal

ar

ch o

n 3

-7 c

m)

Sple

en e

nlar

gem

ent,

hem

orrh

agic

purp

ura

(ecc

hym

osis

, pet

echi

ae

on th

e sk

in),

"vo

miti

ng, c

offe

e gr

ound

s "

Inte

rsti

tial

pne

umon

ia

(sho

rtne

ss o

f br

eath

, cy

anos

is, p

ertu

ssoi

d )

Vom

itin

g, d

iarr

hea,

ab

dom

inal

pai

n

Dar

k ur

ine

Dam

age

of th

e pa

roti

d,

subm

andi

bula

r an

d su

blin

gual

lym

ph n

odes

Localized Generalized

IFA

Acute Chronic

Imm

unom

odul

ator

s:

hype

rim

mun

oglo

buli

n, no

rmal

im

mun

oglo

buli

n hu

man

im

mun

oglo

buli

n an

ticy

tom

egal

ovir

us

Proper personal

hygiene when in contact with

a newborn

38

25

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF MEASLES

Yes No Exanthema. Intoxication syndrome. Catarrhal syndrome.

The rash appears in the first days of illness. Elements of the rash cover all the body. Rash develops simultaneously — small round pink-red spots do not merge and disappear completely after 2–3 days, with no pigmentation or desquamation. Enlargement of occipital and back cervical lymphatic nodes. Subfebrile temperature. Slightly runny nose, cough and sometimes conjunctivitis.

Ru

bel

la

Appearance of the rash is connected with taking sulfonamides, but can be due to other appointed drugs. It appears on the first days after admission. Rash is punctuate. Body temperature increases to subfebrile figures, malaise, also can be itching, swelling, peripheral lymph nodes.

med

icam

enta

l d

erm

atit

is

It begins acutely with vomiting, pain in the throat. The body temperature increases to febrile digits. On the 2nd day of onset appears punctate rash, abundant on hyperemic background, more intense on the sides of trunk, the flexors of the limbs, in the natural folds. The rash does not affect the nasolabial triangle. Peeling starts after the disappearance of the rash. Hyperemia of the stomatopharynx, clearly delimited (catarrhal, follicular, necrotic quinsy). «Strawberry» tongue.

Sca

rlet

fev

er

The disease develops gradually. Itchy nodules and vesicles appear on the skin. There are scabby tracts — linear intradermal inflammatory changes of a few millimeters, usually developing between the toes, on the flexion of the joints, the sides of the back, scrotum. No catarrhal symptoms, normal t.

En

tero

vira

l ex

anth

ema

Sudden onset of the disease, high fever, symptoms of intoxication. From the first hours there are extensive erythematous spots, with huge vesicles. Detachment of the epidermis is observed from the dermis in a large area of the hands, feet and trunk. No catarrhal symptoms.

Lye

ll, s sy

nd

rom

e

Acute onset with high fever (39–40 °C). On the 3 -4 day the temperaturerd th is critically reduced and there is a rash, spreading over the trunk, limbs, neck and head. Pale pink roseola tends to merge keeping for 2–3 days and disappear without desquamation or pigmentation. No catarrhal symptoms. It is commons in elder children.

Six

th d

isea

se

Acute onset of the disease, with the rise of body t to 39 °C and maculosis rash. Pink rash develops on unmodified skin, keeps for 1–2 days, disappears without desquamation or pigmentation. Vomiting and abdominal pain are typical. Scleritis, catarrhal conditions of the upper respiratory tract.

Acute onset of the disease, with the rise of t to 38–39 °C, maculosis papular rash, abundantly located on the face, tending to merge, with pigmentation and desquamation after disappearance. Tonsillitis, lymphadenopathy. Enlarged liver and spleen. –CBC: leukopenia, lymphocytosis, plasma cells.

Infe

ctio

us

mon

onu

cleo

sis

The disease is more frequent in adults. Sometimes it develops after ARI. Primarily, pink-red oval spot appears on the breast with desquamation in the centre. Spots can be found all over the body. Patient’s state is well. Temperature is normal or subfebrile.

Zh

iber

, s p

ink

lich

en

Acute onset of the disease with the rise of t to 38.5-39oС, development of catarrh of upper respiratory tract and conjunctivitis. Grayish-white spots appear on the buccal mucosa. After 4-5 days, maculopapular rash developsin three stages: 1 day —

st

face, neck, 2nd day — trunk, arms, 3 day —rd legs. After the disappearance of the rash brown pigmentation remains and persists up to 1.5 weeks.

Mea

sles

Sca

bie

s

Diagnostic algorithms: measles

Epidemiological

features

Affected

organs

Symptoms

Periods

of disease

Differential

diagnosis

Complications

Peculiarities in

children under 2 years

Diagnostic

Methods

Treatment

Prophylaxis

MEASLES

Instability of the virus Volatility of the virusTransmission —

airborneSource — the patient

Susceptibility - general

Nervous systemThe organs of

digestionSkin Eyes

The respiratory system

Run

ny n

ose,

cou

gh, d

yspn

ea,

retr

acti

on o

f co

mpl

iant

sit

es o

f th

e ch

est

Ena

nthe

ma,

Fil

atov

's sp

ots,

ph

aryn

geal

hyp

erem

ia, w

ater

y st

ool

Feve

r, h

eada

che,

flac

cidi

ty, v

agot

onia

Mac

ulop

apul

ar r

ash,

unc

hang

ed

back

grou

nd o

f ski

n, s

tage

s of

ras

h,

desq

uam

atio

n, p

igm

enta

tion

Phot

opho

bia,

hyp

erem

ia o

f co

njun

ctiv

a, te

arin

g an

d pa

sty

eyel

ids

EruptionProdromal Pigmentation

Flu, adenoviral infection,

paraflu, croup diphtheric

Rubella, scarlet fever, allergic

rash

Stomatitis MeningitisPneumoniaCroup Encephalitis Keratitis

Develops often, during the prodrome

Early, severe

Hemagglutinati on inhibition

reactionBlood analysis

Immunofluorescence

DesensitizationAntibiotics for complications

Care Vitamins

Air changeEarly isolation

of patients8–21 day

quarantineVaccination Gammaglobulin

Symptomatic

26

35

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSTICS OF EPIDEMIC PAROTITIS (MUMPS INFECTION)

Yes No Parotid and salivary glands. Intoxication.

It is more often seen in the elderly. Salivary gland is painful. Swelling is on the affected side. Process is unilateral. There is no fever. The stones that obstruct salivary duct can be revealed by ultrasound (US) and sialography. Normal CBC.

Sal

ivol

ith

iasi

s

Acute onset of the disease, the symptoms of intoxication are expressed slightly. The tonsils are moderately swollen, mild redness of tonsils and palatine arches. There are fibrinous coats on tonsils, «+» tissue, dirty gray, difficult to separate. The subja-cent tissue bleeds when it is removed. The membra-nous coats drown in water, are not grounded between glass slides. Regional lymph nodes are mild swollen and slight painful. In CBC: leukocytosis with neutrophilic shift.

Dip

hth

eria

of t

he

ton

sils

The lesion of the parotid salivary glands occurs due to local purulent infection (otitis, tonsillitis, and dental caries). Acute onset of the disease with high intoxication. Soreness and density are above the parotid gland. The skin over it is bright hyperemic. There is appearance of fluctuation. There is neutrophilic leukocytosis in CBC

Acu

te p

uru

len

t p

arot

itis

The lesion of the parotid glands is associated with occupational hazard. Acute and chronic poisoning by mercury and lead. Disease affects adults mostly. In children it is extremely rare. Mumps develops slowly, often accompanying with changes of the teeth and gums.

Inflammation of the salivary glands is chronic. Re-lapses occur once a year, alternating with periods of clinical well-being. The disease begins with the rise of body temperature, swelling and pain of the gland. Buccal mucosa is swelled on the affected side. Pus discharges from the parotid duct. Spontaneous disappearance of pain and swelling in 7-20 days.

Acute onset. Symptoms of intoxication. The lesion of the parotid salivary gland usually starts unilateral, after 1–2 days the process moves to the second gland. Moderately painful gland has pasty consistency. The skin above it has normal color. Positive Murso’s symptom, pain by pulling the ear up and ahead, with pressure below the outer edge of the ear canal. Vartonov’s duct is swelled. Other glands are involved in the inflammatory process: submaxillary and sublingual salivary glands, pancreas, mammary gland, gonads, thyroid gland. In clinical blood test: leukopenia and lymphocytosis.

Tox

ic p

arot

itis

P

rim

ary

chro

nic

par

otit

is

Ep

idem

ic p

arot

itis

There is intoxication, lymphadenopathy. Lesions of the tonsils are necrotic and ulcerative. It is often one-sided. Necrosis doesn’t rise above a surface of the tonsils; the surface is uneven, rough. On the 3rd–4th day of illness on necrosis place forms an ulcer crater, covered with a very thin fibrinous coat under which ulcer epithelializes for 8–12 days. Putrid smell of the breath. By microscopy in smears taken from the surface of the tonsils detected spirillum and spindle-form bacilli.

Sim

anov

sky-

Rau

hfu

s to

nsi

l-li

tis

Duration of illness is long (for months). Curve of the temperature has undulating character. Lymph nodes are swollen in all groups. Lymph nodes are enlarged to the size of V–VII, dense, fused with each other and the subjacent tissues - «potatoes in a sack.» Biopsy of lymph node shows Berezovsky–Steinberg’s cells. ly

mp

hogr

anu

lom

ath

osis

There is fever. The posterior pharyngeal wall is much hyperemic, loosened. There is a big amount of thick mucus. The tonsils are swollen, raised to II–III degree, hyperemic. Coats on the tonsils are whitish-yellow, loose, rough, rugged, easily removed and grounded between glass slides. The sharp enlargement of cervical lymph node groups, especially those located on the posterior edge of the sternocleidomastoid muscle. Lymph nodes are dense, elastic, not soldered to each other and the subjacent tissues. Nasopharyngeal tonsils are swollen. A child breathes with a half-open mouth; his voice takes on a nasal tone. Hepatosplenomegaly. In CBC: lymphocytic leukocytosis, elevatedESR, presence of atypical mononuclear cells.

Infe

ctio

us

mon

onu

cleo

sis

Disease is rare as a separate unit. Usually damage of pharynx appears due to ARI. Hypertermia, painful throat. On the tonsils, swollen and hyperemic, appears bluish overlay, rarely they can be found only in the gaps or can be like small island. Overlays partially impregnated with fibrin are difficult to remove. They are easily grounded between glass slides. Diffuse T T T T T T T T T T

bright Thyperemia of the ToropharynxT, T Twithout clear boundaries.T TExpressedT TpolyadenopathyT.

TSta

ph

yloc

occa

l an

gin

a

Diagnostic algorithms : diagnostics of mumps infection

Affected organs

and systems

Symptomsand signs

Methods of

research

36

Differential

diagnosis

Treatment

Epidemiology

and prophylaxis

Mumps infection

Submandibular salivary glands

Parotic salivary glands

The ovaries Testes Mammary

glandsPancreas The brain tunic

Enlargement of the gland, pain on palpation

Enlargement of the glands,

absence of acute inflammation,

pain when chewing, anterior

and posterior

Lower abdominalpain

Enlargement of the organ, pain on palpation

Enlargement of glands

Encircling abdominal pain,

repeated vomiting,

constipation or diarrhea

Headache, repeated vomiting,

occipital muscle tension, Kernig's and Brudzinsky

symptom

General blood analysis — shift to the left of the blood formula

Palpation of the gland —

enlargement in size and pain

Virological research — virus

isolation from blood, from

cerebrospinal fluid

Serological complement

fixation test — a diagnostic

antibody titer to the antigen

Investigation of diastase — elevation of

blood and urine diastase

Investigation of liquor — the

ttransparency of cerebro-spinal fluid,

high pressure of liquor, lymphocytic

pleocytosis, the norm of sugar and

chlorides

External examination — enlargement of

glandular organs

Epidemiological anamnesis — contact with a sick person

Anamnesis of the disease — acute onset of disease

Infectious mononucleosis,

tuberculosis lymphadenitis,

purulent lymphadenitis,

systemic disease of the blood

Surgical diseases of abdominal

organs

Calculous parotitis

Submandibular lymphadenitis, toxic diphtheria

of pharynx, calculous

submacsilit

Meningitis of different etiologies

PolyvitaminsDesensitization

preparations

Antipyretics and analgesics

Bed rest and dry heat on the

organs affected

Antibiotics by indications

Cerebral spinal puncture

Intramuscular 25% solution of

magnesium, 20% glucose solution

intravenously, 5% ascorbic acid intravenously

Current disinfection

Isolation of the patient

Slow development of disease outbreak

Highest incidence inthe cold season

Airborne transmission

Quarantine for 21 days

Daily inspection of the contact

persons

Sanitary and educational work

among the population

Preventive vaccination

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSTICS OF STOMATOPHARYNGEAL DIPHTHERIA

Yes

No The syndrome of quinsy.

Intoxication syndrome.

The disease is caused by hemolytic streptococcus. Increased t, intoxication. Inflammation of the tonsils. Enlarged regional lymph nodes. Severe fever. Two-way process.

Ton

sill

itis

(s

trep

toc.

, st

aph

yl.)

Persons who has no immunity to streptococcal erythrogenic toxin are affected. Hyperemia of the skin

Sca

rlet

fev

er

, micropunctate rashes followed by desquamation of the skin, tachycardia, vomiting. Bright hyperemia of mucus membranes - «burning mouth»; clear, bloodshot tongue («strawberry» tongue). Desquamation is especially marked

No marked symptoms of intoxication, subfebrile t. Sore throat at swallowing is absent or not very marked. The process is usually unilateral. On the first day of mild hyperemia, swelling and an increase in one of the palatine tonsils. Then, on a background of hyperemia, a rounded greyish-white spot about 10 mm in size appears on its surface. On the 2

on the fingers.

nd–3rd day coat is forming at this place, when removing — there is an ulcer. Breath is putrid.

Sim

anov

sky-

Pla

ut-

Vin

cen

ts t

onsi

llit

is

,

Develops after hypothermia or ARI. The process is mainly on the tonsils and regional lymph nodes. Low-grade fever is in the evenings, acrocyanosis, lability of heart rate, orthostatic hypotension, unpleasant sensations in the heart. Pains in the throat. Cohesion of the tonsils with the arches, the presence of scars on the tonsils, sometimes in lacunas with caseous plugs.

Rapid rise of the t, chill, marked toxicosis. Sharp pain in throat when swallowing and even at rest, sometimes painful movement of the head. Trismus chewing muscles limits the opening of the mouth; increased salivation. Examination of the stomatopharynx is difficult. Pharyngoscopy detects unilateral swelling and bulging in the absence of coats on the mucous membrane of the tonsils.

Ch

ron

ic t

onsi

llit

is

Par

aton

sill

itis

High fever, general intoxication, an acute onset of illness. Damage of the tonsils and the enlargement of regional lymph nodes. The appearance of quinsy is lagging behind with respect to time by t increasing, symptoms of general intoxication. Pharynx involvement on the third day and later. Bilateral necrotic changes in the tonsils. Fibrinous coat on the tonsils, does not extend beyond the tonsils. Generalized lymphadenopathy. The liver and spleen may be enlarged. There are atypical mononuclear cells in the blood.

Infe

ctio

us

mon

onu

cleo

sis

The rash, usually erythematous, with the figure of the «butterfly on his face», generalized lymphadenopathy

Lis

teri

osis

, enlarged liver and spleen. There are some patients with purulent meningitis. High fever with large daily scale, septic metastases, secondary purulent foci.

The enlargement of one tonsil, its mucosa membrane is hyperemic. The regional lymph node is moderately enlarged of dense consistency, painless. No pain during swallowing. On the affected tonsil develops necrotic processes, forming a hard chancre. Low-grade fever, slight malady. Changes in the tonsils remain for a very long time without significant dynamics (up to a month or more).

Syp

hil

is

The general condition suffers a little. Body temperature remains normal, rarely subfebrile. Coat associated with the fungus is grayish-white, rarely continuous. It is usually located by separated areas, capturing not only the tonsils, but also the mucosa of the mouth, the posterior pharyngeal wall. The fever and symptoms of intoxication are absent. A common whitish coat is on the mucous membranes of the oropharynx. M

ycot

ic t

onsi

llit

is

High fever, pain at swallowing. The process is unilateral, necrotic. Coat is of grayish color, after its removal there is an ulcer. It is characterized by the formation of buboes. The regional upper anterior cervical lymph nodes are enlarged. Bubo is not soldered to the surrounding tissues, is mobile, the skin over it is not changed. Fluctuation of buboes. It may form a fistula.

Tu

lare

mia

Acute onset of the disease. Fibrinous coat is on the tonsils. Sore throat is absent or expressed only slightly. Coat is difficult to separate. Swelling of the subcutaneous fat neck. Coat is not grounded between the glass slides, drowns in the water. Body

otemperature - 37–38 P PC. When removing the coat, surface of the tonsil bleeds.

TSto

mat

oph

aryn

gea

lT Tdi

hth

eria

p

18

DIAGNOSTIC ALGORITHMS: DIPHTHERIA

Localisation

Clinical

forms

Signs

symptoms

Differential

diagnosis

Complications

Treatment

Especially

at the modern stage

Prophylaxis

Diagnostics

Diphtheria

Pharynx Nose Larynx Eyes

Tox

ic

Hyp

erto

xic

Loc

aliz

ed

Sub

toxi

c

Spr

ead

Sudd

en p

hary

nx e

dem

a, s

prea

d sc

oats

, sw

eet

brea

th, e

dem

a o

f th

e ce

rvic

al ti

ssue

Sudd

en o

nset

, dim

min

g of

con

scio

usne

ss,

wea

knes

s, h

emod

ynam

ic d

istu

rban

ces,

co

ats,

and

ede

ma

in th

e th

roat

Isla

nds

or th

e fi

lmy

coat

s on

the

tons

ils,

m

oder

ate

swel

ling

of

the

lym

ph n

odes

Coa

ts b

eyon

d th

e to

nsil

s, a

mar

ked

incr

ease

in

reg

iona

l lym

ph n

odes

Spre

ad c

oats

in

the

phar

ynx,

ede

ma

of

arou

nd t

he ly

mph

nod

es

Cat

arrh

al-

ulce

rati

ve

Mem

bran

eous

Blo

ody

disc

harg

e, e

xcor

iati

on a

roun

d th

e no

se, s

ores

in th

e th

e na

sal m

ucos

a

Film

on

the

nasa

l sep

tum

Loc

aliz

ed c

roup

Wid

espr

ead

A

Wid

espr

ead

B

Hoa

rsen

ess

to a

phon

ia, r

ough

cou

gh,

sten

osis

I

sten

osis

II

ste

nosi

s II

I

Cat

arrh

al f

orm

Cro

upou

s fo

rm

Dif

teri

tica

l fo

rm

Hyp

erem

ia o

f th

e co

njun

ctiv

a, p

urul

ent

disc

harg

e fr

om th

e ey

es

Mod

erat

e ed

ema

of th

e ey

elid

s, m

embr

anou

sco

njun

ctiv

itis

Sudd

en e

dem

a of

the

eyel

ids,

fil

ms

on

conj

unct

iva

and

on th

e ey

ebal

l

Par

aton

zill

itis

Nec

roti

c an

gina

AR

VI

Ang

ina

Sim

anov

sky

Fal

se-m

embr

anou

s an

gina

Ton

sill

itis

foll

icul

aris

Lac

unar

tons

illi

tis

Epi

dem

ic p

arot

itis

Infe

ctio

us m

omon

onuc

leos

is

Of

nose

for

eign

bod

y

Cro

up f

or A

RV

I

Cro

up in

oth

er in

fect

ions

For

eign

bod

y

Pap

pilo

mat

osis

aden

ovir

al c

onju

ncti

viti

s

Eth

moi

diti

s

Orb

ital

cel

luli

tis

Poly

radi

culo

neur

itis

Para

lysi

s an

d pa

resi

s of

cra

nial

ner

ves

Myo

card

itis

Serotherapy, desensitisation, vitamins, and plasma hormones, magnesium sulfate, strychnine, cocarboxylase, ATA, glutamic acid, dibazol, proserin,

intubation, tracheostomy

Reduction of incidence up to sporadic cases, reducing of mortality, increasing of the coefficient of severity, the prevalence of pharynx diphtheria, lack of periodic rises, the incidence in older children, the

predominant disease in rural areas, bacilli carriers are the main source of infection

Iden

tifi

cati

on o

f ca

rrie

rs o

f to

xige

nic

bact

eria

Mea

sure

s in

the

focu

s of

the

dise

ase

Con

trol

of

imm

unit

y

Tre

atm

ent o

f ca

rrie

rs

Act

ive

imm

uniz

atio

n

Bac

teri

olog

ical

res

earc

h

Ser

olog

ical

rese

arch

Bac

teri

osco

py s

wab

Pano

phta

lmia

19

Infrequent localisation

Dif

teri

tica

l fo

rmco

njun

ctiv

a an

d on

the

eyeb

all

Orb

ital

cel

luli

tis

19

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF INFECTIOUS MONONUCLEOSIS

Yes No Intoxication. Tonsillitis.

Adenosplenomegaliya.

There is fever. The symptoms of catarrh of the upper respiratory tract: an abundant mucous purulent discharge from the nose, mild hyperemia of the posterior pharyngeal wall. Typical eye disease - purulent conjunctivitis. There is a hyperplasia of lymphoid formations of oropharynx. Swollen lymph nodes of the neck. Normal CBC. A

den

ovir

al

infe

ctio

n

There is fever. There are severe catarrhal conditions of the upper respiratory tract infections. The phenomena of diffuse bronchitis. Loss of appetite, dyspepsia, colitis, a significant increase in liver, spleen, and a slow return dynamics. Hypochromic anemia. A significant increase of ESR, leukocytosis is often observed. The pain is in the abdomen. Isolation of the pathogen from blood, bone marrow, stool, bile. Serological methods: Rayt - Heddelson’s reaction

Bru

cell

osis

shows the growth of antibody titer of Brucella 1:200. Acute onset of the disease. Symptoms of intoxication are expressed only slightly. Swelling of the tonsils is moderate, mild hyperemia of the tonsils and palatine arches. On the tonsils fibrinous mem-branous coats “+ tissue” of dirty-gray color, difficult to separate. The subjacent tissues bleed when they are removed. The membranous coats are drowning in water, grounded between glass slides. There is a moderate increase and slight tenderness of regional lymph nodes.

Prolonged subfebrilitis, lymphadenopathy, enlarged liver and spleen, severe muscle pain, generalized arthralgia without visible changes in the joints. Chorioretinitis, progressive myopia. Changes of the autonomic nervous system. Detection of calcifications in the bone marrow by the X-ray. Serological study shows the growth of Toxoplasma antibodies titer.

Tox

opla

smos

is

In general blood analysis:

dip

hth

eria

S

tom

atop

har

ynge

al

leukocytosis, neutrophilic shift.

Intoxication. Poliadenopathy. Necrotic and ulcerative lesions of the tonsils, usually on one side. Necrosis does not rise above the surface of the tonsils, its surface is uneven, rough. On 3-4 days of illness ulcer crater is formed on the place of necrosis, covered with thin coats of fibrinous film, under which for 8-12 days, an ulcer epithelialized. There is putrid breath. In smears taken from the surface of the tonsils, the microscopy detectd spirillum and spindle-shaped bacilli.

Sim

anov

sky-

Pla

ut-

Vin

cen

t, s to

nsi

liti

s

Long period of disease (for months). The temperature curve is of undulating nature. Lymph nodes are increased in all groups. Lymph nodes are enlarged to the size of VI-VII, tight, welded together and the underlying tissues. Symptom "of potatoes in a sack." Biopsy detects cells of Berezovsky-Steinberg in the lymph.

Lym

ph

ogra

nu

lom

atos

is

Sharp paleness of the skin. Enlargement of the spleen.

Long-term subfebrile fever. Fatigue, lymphadenopathy, weight loss, persistent cough, diarrhea syndrome. Damage of the upper gastrointestinal tract by the fungi of genus Candida. Pneumocystis pneumonia. Disruption of the central nervous system. Kaposi's syndrome. Reducing

Increased bleeding, reduction in the number of red blood cells and hemoglobin, significant increase of ESR.

Acu

te le

uk

emia

The results of sternal puncture: increased

AID

S

myelokaryocytes, reducednumber of metakariocytes, impaired myelopoesis. Sharp increase in the number of

number of T-lymphocytes.

blast cells, decreased amount of intermediate and mature forms of myeloid.

Infe

ctio

us

mon

onu

cleo

sis

The fever. The posterior pharyngeal wall is very hyperemic, loosened with a large number of thick mucus

20

. The tonsils are swollen, raised to II-III degree, hyperemic. On the tonsils there are whitish-yellow coats, loose, rough, easily removed, and the subcutaneous tissues do not bleed. Incrustations easily pounded between the slides, do not sink in water. The sharp increase in cervical lymph node groups, especially those located on the posterior edge of the sternocleidomastoid muscle. Lymph nodes are dense, elastic, not soldered to each other and the subcutaneous tissues. Swelling of nasopharyngeal tonsils. The child breathes with half-open mouth; his voice takes on a nasal tone, pasty eyelids. Hepatosplenomegaly. In CBC: lymphocytic leukocytosis, elevated ESR, presence of atypical mononuclear cells.

Diagnostic algorithms : Infectious mononucleosis

Affected organs

systems

Symptoms

and signs

Methods

of diagnosis

Diagnostic

features

Differential

diagnosis

Especially

in infants

Treatment

Infectious mononucleosis

Lymph nodes Nasopharynx Pharynx Parenchymal organs Blood

Enlargement of lymph nodes,

enlargement of all groups of lymph

nodes

Difficulty of nasal breathing

QuinsyEnlarged liver and

spleenFever

Palpation, external examination

Anterior and posterior rhinoscopy

Cytology of the tonsils,

pharyngoscope, bacteriological

examination

Palpation, biochemical research

General blood an alysis, leuko-concentrate,

serological reactions,thermometry

Sca

nty

runn

y no

se, e

nlar

gem

ent o

f na

soph

aryn

geal

tons

ils,

coa

ting

in th

e na

soph

aryn

x, a

typi

cal m

onon

ucle

ar c

ells

in th

e sm

ear,

cat

arrh

al p

heno

men

a, c

oatin

hin

the

phar

ynx

Min

or b

ioch

emic

al c

hang

es, m

ild

leuk

ocyt

osis

, mon

onuc

leos

is, a

typi

cal m

onon

ucle

ace

lls,

mod

erat

ely

acce

lera

ted

ES

R

The

rea

ctio

n of

Pau

l-B

unne

lya-

Dav

idso

n, th

e re

acti

on o

f T

omcz

yk, h

emag

glut

inat

io te

st w

ith

hors

e er

ythr

ocyt

es

A lo

t of

mov

ing,

wit

hout

pai

nful

lym

ph n

odes

, no

infl

amm

atio

n, c

ellu

lar

tiss

ue

past

osit

y

Acu

te o

nset

, sor

e th

roat

, sno

ring

bre

athi

ng, c

hang

es in

the

conf

igur

atio

n ne

ck, l

ong-

term

hig

h te

mpe

ratu

re

LymphadenitisTonsillitisPharynx diphtheriaAcute leukemiaLymphogranulomato

sisViral hepatitis

Adenoviral infection,HIV infection

Significant damage of nasopharynx, expressed catarrhal phenomena, skin eruptions, more atypical mononuclear cells in the blood, the absence of serological changes, insignificant coating on the tonsils

AntihistaminesAntibiotics(indicated)

AntipyreticVitaminsCorticosteroids

(indicated)

21

33

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF SCARLET FEVER

Yes No Micropunctate exanthema. Syndrome of tonsillitis. Intoxication.

The rash appears on the 3rd -4 day of onset. The skin is hyperemic. Hyperemia and expressed skin pastosity of hands and feet (the symptoms of "gloves", "socks", "hood"). There is a moderate hyperemia in the pharynx. "Strawberry" tongue. Hepatosplenomegaly. There are muscle and joint pain. Micropunctate rash is on unmodified skin, usually in the abdomen, axillary region, on the lateral surfaces of the body.

th

Pse

ud

otu

ber

culo

sis

Maculo-papular rash, maculosis, catarrhal conditions, subfebrile temperature. The rash stag-ing on the hyperemic background skin is specific. The pigmentation is after the disappearance of the rash. Filatov-Koplik,s spots, conjunctivitis. Sometimes croup syndrome may develop, rash tends to merge.

Mea

sles

It begins acutely, temperature rises, catarrhal symptoms appear. Lymphadenopathy - cervical, back cervical, located behind of sternocleidomastoid muscle like a chain. There are tonsillitis and hepatosplenomegaly. In CBC: atypical mononuclear cells, increased ALT, AST. Jaundice. Maculosis rash, and then can be pigmentation, skin desquamation.

Catarrhal symptoms. Polymorphous rash, maculopapular, hemorrhagic, often around the joints (in the hands, feet) (a symptom of "gloves", "socks", "hood"). Joint inflammation (swelling, redness, tenderness, limitation of movement). Myocarditis. Hepatosplenomegaly. Nausea, vomiting, and abdominal pain. Pouring sweat, high fever, with large daily fluctuation. Jaundice, diarrhea. Stool diluted, often with mucus, green, sometimes blood.

Infe

ctio

us

mon

onu

cleo

sis

inte

stin

al y

ersi

nio

sis

Acute onset, high fever up to 39oC and more. The rash is small maculosis -papular. Headache, muscle pain, scleritis, catarrhal symptoms. Vomiting and abdominal pain are typical. Localization of rash: face, body, sometimes arms and legs. Rash is on unmodified background skin. Rash doesn’t have staging, doesn’t leave pigmentation or desquamation.

En

tero

viru

s b

osto

n

exan

them

a

Maculosis rash associated with taking sulfonamides, antibiotics. General malaise, fever, often to subfebrile. Itching of the skin, enlargement of peripheral lymph nodes. In the blood: mild eosinophilia. The rash tends to merge, no staging. Rash appears during the first days of drug administration.

Med

ical

der

mat

itis

Normal or subfebrile t. Rash is maculosis, abundant, most marked on thetrunk. Single rosella and papules are revealed. The rash persists for a long time up to 2-3 weeks, then gradually fades and disappears without a trace. Anamnesis: the presence of primary syphilides (chancre) residual effects. Rash appears on a relatively good state of health of the patient, long-term preservation of rash without dynamic.

Syp

hil

is

The disease is most often seen in young children. The rash is micropunctate, single, with a hemorrhagic component, localized on the face, neck, upper body. Manifestations of disseminated intravascular coagulation (DIC). Diagnosis is based on severe clinic of flu. T

oxic

for

m o

f in

flu

enza

Catarrhal symptoms. Micropunctate rash is followed by desquamation of the skin. Tachycardia, frequent vomiting. Bright redness of the throat - "flaming" pharynx. Rash is on hyperemic skin, especially on fingers. Tonsillitis, lymphadenopathy, "Strawberry" tongue. Rash doesn’t leave pigmentation. Pale nasolabial triangle. Thickening of the rash on the cheeks, T T T T T

Ton the side ofT Tthe trunk,T Tabdomen,T TflexorT Tsurfaces of limbsT.

Sca

rlet

fev

er

Body temperature is subfebrile. The rash is small maculosis, sometimes papular, disappears without pigmentation, desquamation, and does not tend to merge. There is no rash staging. Lymph nodes are swollen - occipital, back cervical. slight conjunctivitis. In CBC: leukopenia, relative lymphocytosis, plasma cells (10-30%).

Ru

bel

la

DIAGNOSTIC ALGORITHMS: scarlet fever

Type of the course

Clinical

forms

Signs and

symptoms

peculiarities

in babies

Differential

diagnosis

Character of the course

Complications

Treatment

Prophylaxis

Scarlet fever

typical atypical

Severe toxic

Severe septic

Medium-severe

MildToxic-septic

Extra-pharynge

al

Hypertoxic

Hemorrhagic

Obliterated

t ris

e to

38C

, si

ngle

vo

mit

ing,

cat

arrh

al to

nsil

liti

s

t ris

e to

40

°C, r

epea

ted

vom

itin

g, n

ecro

tic

tons

illi

tis

t ris

e to

41C

,cra

mps

, del

iriu

m,

men

ingo

-enc

epha

litic

syn

drom

e

Sep

tice

mia

, phl

egm

onou

s ad

enit

is,

pyos

epti

cem

ia, e

xten

sive

nec

rosi

s in

th

e or

opha

rynx

, enl

arge

men

t of

the

live

r an

d sp

leen

Man

ifes

tati

on o

f to

xic

and

sept

ic f

orm

s

Cat

arrh

al q

uins

y,

subf

ebri

liti

s, s

atur

atio

n, s

kin

fold

s

Wou

nd s

urfa

ce, r

egio

nal

rash

, abs

ence

of

quin

sy

Unc

onsc

ious

ness

, cra

mps

, pa

raly

sis

of s

ympa

thet

ic,

coll

apse

Hem

orrh

agic

syn

drom

e,

seve

re in

toxi

cati

on

Low incidence, intoxication is weakly expressed, the absence of severe toxic forms, the severity of septic process in the acute period, the frequent development of septic

complications, rare allergic complications

Rubella MeaslesChickenp

ox rash

Allergic rash

Scarlet fever like

Far Eastern fever

Staphylococcal infection with scarlet fever like syndrome

QuinsyPharynx

diphtheriaSudamen Flu

With complications

Smooth With allergic

waves

Lym

phad

enit

is

Oti

tis

Mas

toid

itis

Sinu

siti

s

Nep

hrit

is

Syno

viti

s

Symptomatic: antipyretic, cardiacs,

antihistamines

Etiotropic: antibiotics

Liquid injection, plasma injection

One-stage filling of the chambers

QuarantineIsolation Disinfection

34

27

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF MENINGOCOCCAL INFECTION (PURULENT MENINGITIS)

Yes No Meningeal syndrome. Hypertension. Intoxication.

Acute onset of the disease with febrile fever, violent headache, hyperesthesia, repeated vomiting, and intoxication increases. A large fontanelle protrudes, sutures do not hold, size of the skull is increasing, loss of consciousness, convulsions, mono- and hemipareses. Focal lesions appear on 1-2 days of illness. Cerebrospinal fluid is muddy, often greenish, neutrophilic pleocytosis (500-1500) 106/l, increase in protein (1-10 g/l).

Pn

eum

ococ

cal

men

ingi

tis

Meningeal syndrome is developing after exanthema and is accompanied by a sharp rise in temperature to 40°C, nausea, vomiting, severe headache, hyperesthesia. Meningeal symptoms, decreased or absent tendon reflexes, especially in the lower extremities. The abdominal reflexes are absent or reduced. Cerebrospinal fluid flows under high pressure, cytosis (60-150) .106/l, lymphocytes predominate. The protein content is slightly increased (1.5 times).

Mea

sles

m

enin

goen

cep

hal

itis

Signs of meningoencephalitis appear soon after the disappearance of the rash. Low-grade fever, enlarged occipital and back cervical lymph nodes. Headache, vomiting, disturbances of consciousness, tonoclonic convulsions. Paresis, ataxia, central respiratory disorders. In cerebrospinal fluid dominated amount of lymphocytes is revealed. Virological methods - virus allocation from blood.

Ru

bel

la

men

ingo

ence

ph

alit

is

Acute onset of the disease, with a rise in t to 38-40oC. CNS damage is preceded by parotitis, an inflammation of other glandular organs. Severe headache, vomiting, weakness, myalgia, moderate meningeal syndrome. Cerebrospinal fluid flows under pressure, the protein content is normal or increased to 2.5 g/l, cytosis is from several hundreds to 2000,10 /l6 at the expense of lymphocytes, a film of fibrin may fall.

Par

otid

m

enin

giti

s

The disease begins acutely, with a rise in body temperature to 39-40oC. There is a severe headache, dizziness, repeated vomiting, restlessness, and sometimes abdominal pain, delirium, convulsions. The patient's face is hyperemic, slightly pasty, injected scleras. Mucus membranes of oropharynx are hyperemic, grain on the back wall of the pharynx and soft palate. Meningeal symptoms are from the first day, short-term. Liquor of spinal puncture is transparent, cytosis of 200-300 cells per 1 mm3 flows under the pressure; cytosis is firstly mixed, then the lymphocytic. The Pandey s reaction, is weakly positive.

En

tero

viru

s in

fect

ion

(s

erou

s m

enin

giti

s) Headache, repeated vomiting, shuddering and

twitching of individual muscle groups and limbs, and sometimes tremor, horizontal nystagmus. Meningeal symptoms are on 2-3 days of illness. In the liquor lymphocytic cell count is moderate (up to 200-300 mm3 in 1 mm), a slight increase in protein. Paralysis does not develop, but there is weakness when walking.

Pol

iom

yeli

tis

men

inge

al f

orm

It develops more often in the presence of influenza. It is characterized by an identical clinical picture of meningitis, but in contrast to recent positive dynamics is observed fast after the lumbar puncture. Liquor is diluted, from the general blood analysis - picture of a viral infection. M

enin

gism

M

enin

goco

ccal

m

enin

giti

s

Occurs on the 7 -9 day of vaccinationth th , withhigh temperature. Generalized tonoclonic convulsions, anxiety, tremors, motor automatisms, tremor of the extremities, anizoreflexia, pyramidal signs. Hallucinatory-delirium syndrome, psycho disorders, cataleptic phenomena. Normal CSF.

Pos

tvac

cin

al

men

ingo

ence

ph

alit

is

The disease begins with a rise in temperature to 39-40oC, strong chill. Severe headache, becoming worse when moving head, strong stimuli. Marked hyperesthesia, repeated vomiting, and convulsions. Meningeal symptoms for 2-3 days, red dermographism. In the spinal puncture - CSF is turbid, putrid, neutrophilic pleocytosis, measured from thousands of cells in 1 microlitre.

Algorithms of treatment: meningococcosis

Affected organs

and systems

Clinical

forms

Clinical

symptoms

Similar

diseases

Methods

of examination

Treatment

Epidemiology

and prophylaxis

Meningococcosis

CNS Skin Paranephroses Nasopharynx

Bacteria carryingMeningitis Meningococcemia Nasopharyngitis

Nuchal rigidity, Kernig's symptoms

and Brudzincski symptoms,

hyperesthesia, convulsions, red dermographism

Stella hemorrhagic rash, maculopapular rash, arthritis, uveitis

Hyperemia, cyanosis ofthe skin, cold

extremities, dullness of the heart sounds,

tachycardia, falling blood pressure

Rhinitis, hyperemia of the throat

Meningoencephalitis, secondary purulent meningitis, mumps

meningitis, enteroviral meningitis, tuberculous

meningitis, food toxic infection (FTI), the brain commotion

Toxic flu, hemorrhagic vasculitis, scarlet

fever, measles, rubella, sepsis

ARVI

Bacteriological examination — the

discharge of meningococcus

Cerebrospinal fluid — high cerebrospinal

pressure is cloudy, highprotein + Pandy

reaction, high cytosis, neutrophilous citosis,

discharge of meningococcus

Epidemiological investigation

Thick drop of blood — the discharge of meningococcus

CBC: high leukocytosis,

neutrophilia, shift to the left, increased ESR

DesensitizationDehydrationDeintoxication Anticonvulsant CorticosteroidsAntibacterial Diuretics

Examination of all contactsIsolation of patient

Age, seasonality, periodicity

Isolation and treatment of a person

discharging bacteriaCurrent disinfection

28

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF PERTUSSIS, PARAPERTUSSIS

Yes No

22

Syndrome of intoxication.

Paroxysmal cough.

Intoxication is moderate. Night sweats, weight loss. Polymicroadenopathy. Constant dry non-productive cough, rare or frequent. Marked tachypnea with tachycardia. Change in chest radiographic findings. Positive tuberculin test.

Acu

te m

ilia

ry

pu

lmon

ary

tub

ercu

losi

s

Due to the sudden closure of the glottis a child stops breathing, turns blue, cyanosis is gradually

Lar

yngo

spas

m

replaced by pallor, and sweat appears on his face. After the attack - a deep breath. Mild in-spiratory dyspnea may persist.

The disease begins gradually. During the whole period of the disease – subfebrile t. Intoxication is weak. Rhinitis and pharyngitis aretypical. Laryngitis is especially marked. Symptoms of croup often develops in young children - dyspnea, barking cough, hoarse voice.

Par

ain

flu

enza

The correct diagnosis is made after laryngoscopy. The cough is chronic and hoarse. Depending on the location of the tumor there is change of voice, inspiratory dyspnea with stridor. Dyspnea is chronic.

Lar

ynge

al d

iph

ther

ia

(dip

hth

erit

iccr

oup

)

Cough is spastic and paroxysmal. Asphyxia occurs in severe cases. The attack occurs suddenly in absolutely healthy person; the exact time of its occurrence is said. At first the cough is dry. Then when connecting a secondary infection, it becomes wet, paroxysmal. Sometimes it is possible to establish the movement of a foreign body in the trachea at distance, or in auscultation. In bronchial obstruction there is the development of atelectasis. F

orei

gn b

ody

The attack occurs more often at night. It is preceded by a period of precursors which are anxiety, sleep disturbance, excitement. Typical autonomic disturbances are pallor or flushing, sweating, headache. Phenomena of respiratory discomfort appear: throat irritation, chest tightness, stuffiness in nose, sneezing. Then the troublesome attacks ofcough, sibilant rales, heard at distance, dyspnea with difficult expiration occur. After attack there is viscous and glassy expectoration. At microscopy there are eosinophils, asthma crystals and Curschmann's spirals in sputum.

Bro

nch

ial a

sth

ma

Clinical picture develops gradually. Mild symptoms of intoxication. The appearance of rough barking cough, slight hoarseness - stage croupous cough. Later symptoms of croup are progressing steadily - the disease passes into the second stage - the stenosis. Breathing is difficult, noisy breathing, aphonia, silent cough. Development of the II-III stages of stenosis.

There is rhinitis at the beginning of the disease. Laryngotracheitis. Cough becomes worse at the end of the 2 weeknd . It is characterized by the absence of marked fever. General condition is relatively good. Assiduous increasing cough. Passive hemagglutination test (PHT) with parapertussis diagnosticum is positive. P

arap

ertu

ssis

When you go out to the street compensatory cough develops because of reflex spasm of the larynx. There are no symptoms of intoxication, catarrhal symptoms. There are repeated cases of such phenomena in the past C

old

all

ergy

history

Lar

ynge

al

pap

illo

ma

Paroxysmal spasmodic cough is characterized by a long sequence of coughing strength on exhale, after which there is a noisy inspiration - and a new series of coughing strength. Attacks of cough end with the discharge of viscous ropy expectoration, vomiting. In older children before the attack of cough there are phenomena of precursors. There are conjunctival hemorrhages in the eyes, puffiness of the face, aphthaes on the frenulum of the tongue. There is leukocytosis, lymphocytosis, reduced ESR in CBC.

Per

tuss

is

DIAGNOSTIC ALGORITHMS : PARA WHOOPING COUGH

Etiology

Seasonality

Mechanism

of transmission

Affected organs

and tissues

Clinical forms

Methods of diagnosis

Differential

diagnosis

Principles of treatment

Prophylaxis

PARA WHOOPING COUGH

bacillus of parawhooping cough

Autumn-winter

Airways (bronchi, trachea, alveoli)

CNSLungs

(pneumonia)Eyes

Com

puls

ive

coug

h, s

ligh

tly r

unny

nos

e , r

epri

se, t

he

paro

xysm

s, th

e di

scha

rgin

g of

vis

cous

muc

us, s

ore

offr

enul

um o

f th

e to

ngue

cere

bral

hem

orra

ge, h

ypox

ic e

ncep

halo

path

y,

conv

ulsi

ons,

men

ingi

smus

Pne

umon

ia, s

egm

enta

l ate

lect

asis

and

equ

ity,

em

phys

ema

Ble

edin

g in

the

eye

conj

unct

iva

Epidemiological (contact with

patients, bacteriocarriers)

Clinical

Haematological (leukocytosis,

lymphocytosis)

serologic (CFT, agglutination test

pertussis like Subclinical

Bacteriological (detection of

bacilli of parawhooping

cough)

Prodrome of measles

Croup Bronchial asthma Foreign body Whooping coughBronchitis PneumoniaRespiratory allergoses

ARVI

Neuroleptics Oxygen therapyAerosols: mucolytics, proteolytics (trypsin,

chymotrypsin), antispasmodics (aminophylline,

ephedrine)

Antihistamines

Aminazine 2.5%

Dimedrol, prometasine,

suprastin

Isolation of patients Sanitary-hygienic

regimen

Dispensary observation

Airborne

23

DIAGNOSTIC ALGORITHMS : WHOOPING COUGH

Periods

Clinical

symptoms

The differential

diagnosis

Methods

of diagnosis

Especially in

infants

Complication

Principles

of therapy

Especially at

the present stage

Prophylaxis

WHOOPING COUGH

Incubatory Catarrhal Spasmodic

coughPermission

Temperature is normal or subfebrile,

obsessive cough, slight effects of

catarrh of the upper respiratory

tract

Discharge of viscous mucus,

paroxysmal cough,

rinspiratory whoop, vomiting after coughing,

variated wheezing in the lungs, sores on the frenulum of tongue, scleral

hemorrhage

Pulmonary emphysema,

hyperexcitability, occasional bouts

of coughing

ARVI, bronchitis, premonitory symptoms of

measles

Croup, bronchial asthma, foreign

body, tuberculosis

bronhoadenit, respiratory

allergosis, a para whooping cough,

pneumonia

Clinical — paroxysmal

cough, normal temperature, and atelectasis in the

lungs, the b f

Epidemiologic — contact with the

sick and coughing

Hematologic — evalution of leucocytes

degree, lymphocytosis,

normal ESR

Serologic — complement

fixation, agglutination test,

reaction of slowed

h l ti ti

Bacteriological — culturing bacillus of Bordetella pertussis

Other — skin test, the method

of immunofluoresce

nce

Shortening of the catarrhal period, absense of respiratory whoop, attack of cyanosis, apnea, cough equivalents, undulating course and frequent

complications

Pneumonia Encephalopathy Otitis Sinusitis Other

The optimal regimen

Aerial oxygenation therapy

Antibiotics Neuroplegics Aerosol inhalationDesensitization and

symptomatic medication

Reducing of morbidity rate, elimination of mortality, age susceptibility, frequency of abortiveobliterated forms pertussislike

disease, contagious index bacteriocarrier, strong immunity


QuarantineBacteriological examination of

contact

Active immunization

24

51

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF DYSENTERY

Yes No Intoxication, invasive diarrhea

Acute onset of the disease, characterized by the gradual development and intensification of symptoms within 3-4 days. From the first day of the disease there is a significant amount of mucus, blood, its color is dark green, it becomes frothy, like "swampy slime." Vomiting is not often, but persistent. The body temperature rises from the 1st day of illness, reaching a peak in the first 3 days and lasts at average 5-7 days. There is enlargement of the liver and spleen. S

alm

onel

losi

s of

en

tero

kol

itic

for

m Acute onset of the disease with fever. Stool is

frequent,10-15 times a day, watery, yellow or orange, with an admixture of small amounts of mucus, without blood. The abdomen is moderately distended; soft, abdominal murmur is along the small intestine. The liver and spleen are not enlarged. The anus is closed, there is an irritation around it and on the buttocks. Vomiting is persistent, but not often, 2-3 times a day. Regurgitation.

Esc

her

ich

iosi

s en

tero

pat

hog

enic

for

m

Acute onset of the disease, with a rise in body temperature, there is periodical cramping abdominal pain. Symptoms of intoxication are observed in the first 1-2 days, maximum - 3 days. Diarrhea is up to 5 times a day, sometimes - 10 times, quite profuse with a great amount of mucus, and blood-streaked. Anal sphincteris closed, there is no tenesmus.

Esc

her

ich

iosi

s en

tero

inva

zive

for

m

Acute onset of the disease, with rising t up to 37.5-38-39oC. Vomit is abundant, mixed with food, and then - watery, with flakes of mucus. Stool becomes frequent up to 5-15 times a day, watery, bulky, yellow or yellow-green, frothy, with a pungent odor, splash-stool. Sometimes it is a dull whitish or pityriasis. Pain is cramping in the epigastric or umbilical region. The mucous membrane of the soft palate, small tongue, palatine arches are partially hyperemic and slightly swollen, grainity. The liver and spleen are not enlarged.

The disease begins acutely, with liquid stools. It becomes colorless, watery and bulky, with floating flakes, like “rice water”, there is no peculiar smell, mixed with mucus and blood, up to 3-10 times a day. Vomiting starts after the diarrhea. Temperature is decreased or subfebrile. Imperative feeling of defeca-tion are frequentat night.

Ch

oler

a

There are complaints of abdominal pain, usually on the left side, bloating, borborygmus, and constipation. The stool may be like to "sheep-dung" or its first portions are formed, following – liquid (constipational diarrhea). Defecation is divided into two parts: patient feels defecation urge straight after defecation. There is mucus, and sometimes blood in feces. There is loss of appetite, and sleep disturbance. Nausea and vomiting are not typical. There is no fever. U

lcer

ativ

e co

liti

s

Acute onset of the disease, with rising t up to 38 -39oС. There are florid symptoms of intoxication. Nausea, repeated vomiting and abdominal pain. Frequent stool: from 2-3 to 15 times a day, often with mucus and blood. The abdomen is moderately distended. Sometimes the liver and spleen are enlarged. Sometimes there are catarrhal signs, in some cases - polymorphic eruption on the skin around the joints, on the hands, and feet.

Inte

stin

al y

ersi

nio

sis

The disease begins acutely, with body temperature rising up to 38-39-40 ° C, repeated vomiting, but not often. Anorexia, chills, myalgia, and joint pains. There is abdominal pain, it is located around the omphalus and on the right side, it becomes worse worse before defecation. Diarrhea occurs on the first day, watery, fetid, from 2-5 up to 20 times a day. On the 2nd day there is a large amount of admixtures of mucus, and blood. C

amp

ylob

acte

rios

is

Rot

avir

us

gast

roen

teri

tis

Acute onset of the disease, with rising t to 38-39oC, which lasts no more than 3 days. Frequent single or repeated vomiting. Headache, cramping abdominal pain, usually moderate, without distinct localization. Stool becomes more frequent, it becomes liquid, with mucus and blood. First, the stool is formed, and then at 2-3 day feces disappear completely, stool becomes scanty like the "rectal" spit - a lump of mucus and blood. Tenesmus. Sigmoid colon is spasmed. Compliance of the anus. D

ysen

tery

Acute onset of the disease. There are regurgitations, vomiting, stop weight gain and diarrhea. Stool becomes more frequent up to 5-8 times a day. Fecal matters aren’t nonhomogenous, liquid, yellow-green color, with mucus and white lumps, with an unpleasant odor. During expressed meteorism stool is spitting. There is irritation of the skin around the anus. There is offensive breath, meteorism, tongue is coated. There is no temperature E

asy

dys

pep

sia

Diagostic algorithms: dysentery

Epidemiological

characteristics

of dysentery

Classification

Forms

Clinical

symptoms

Flow 52

Outcomes

Differential

diagnosis

Methods

of diagnosis

Especially in

children of

the first year of life

Principles

of treatment

Prophylaxis

DYSENTERY

Waterway Food way Contact wayFlattening of

seasonal curveNo expressed

immunity

Predominance of thedisease by 1–3

Late admissionTypical forms Atypical forms

Easy Moderately Severe

t increases up to 37.5C, vomiting — 1 time/day,

stool is up to 5–8 times/day

t 37.5–38 C, repeated vomiting, appetite disorders, sleep disturbances, atony, spontaneous

abdominal pain, frequent stool up to

10–15 times/day

Temperature is above 38.5,

repeated vomiting, convulsions,

unconsciousness, persistent

abdominal pain, incompletely closed

anus, the stool is

DyspepticSubclinicalHypertoxic

Hyperthermia, unconsciousness,

meningo-encephalitic

syndrome, a drop in blood pressure,

cyanosis, pulmonary

emphysema, heart

Absence of intoxication, a

stool is up to 1–2 times, porridge-

like, compliances of

anus

Subfebrile temperature,

dyspeptic disorder of

defecation, there is no pliability

the anus or spasm of the

Subacute to 1.5 months

Acute 15–21 dayProlonged more than 1.5 months

Chronic, more than 3 months

Abbreviative 1–3 days

Bacterial carryingBowel

dysfunctionPost-dysenteric

colitisRecovery

InvaginationAppendicitisCholeraColiinfectionSalmonellosis Meningitis Dyspepsia Enzimopaty Staphylococcal infection

of the intestinal tract

Luminescent microscopy

CoprogramBacteriological

researchSerological reactions

Crying, blushBlood appears in

3–5 daysThere is no toxic

formStraining before

deficationThere is no spasm

of sigm

Desensitizing therapy

DietAntibiotic

therapyDetoxication

therapyDehydration

therapyBiopreparations

Symptomatic therapy

Terminal disinfection

Bacteriological examination

discharging bacteria

Identification and isolation of patients

and people

Compliance with the rules of personal and

public hygiene

Monitoring of patient's contacts

Educative activities

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF INTESTINAL COLI-INFECTION IN INFANTS

Yes No The enteritis syndrome, intoxication

Disease occurs in infants and is caused by intro-ducing of supplementary food or transferring the child to bottle feeding. In such cases, when the process is too rapid, or when the quantity and quality of introduced supplementary food is not adequate to the child’s age, it leads to the functional disorders of intestines. There is no intoxication, regurgitation. Child is relatively calm. Unformedstool without pathological addi-tive. All disorders disappear after the elimination of

Temperature of the body increases from the first day of the disease to subfebrile digits. Rash is micropunctate, located in the armpits, chest, morbilliform rash in the joints. Symptoms of intoxication, nausea, vomitinggeneralized abdominal pain. Stool is porridge-like, with a small amount of mucus 3-6 times day. The disease is often accompanied by respiratory syndrome, hepatosple

Inte

stin

al

yers

inio

sis

Eas

y d

ysp

epsi

a

,

a

nomegaly.

all nutritional causes

The disease occurs in infants. It is related with mother’s disease (mastitis, sore throat, etc.). The disease develops gradually. Stool becomes more frequent, liquid, with mucus, green, often blood-streaked. The temperature is subfebrile. Clinical course is an undulating, with prolonged (for several weeks), subfebrile fever, unstable stool.

Sta

ph

yloc

occa

l en

teri

tis

Temperature increases, symptoms of intoxication, nausea, repeated vomiting, and anorexia. Abdominal pain becomes worse before defecation. Stool is liquid, watery,

Cam

pyl

obac

teri

osis

frothy, mixed with mucus and blood.

It occurs in infants, prematurity and being bottle-fed. Disease begins acutely. Vomiting, abdominal pain, loose stools with admixtures of mucus and blood. The liver is enlarged. Unlike to dysentery there is no the tenesmus and compliance of the anus.

salm

onel

losi

s,

coli

tic

form

.

The disease is more common in children younger than 2 years. The body temperature is up to 37-38°C. There are symptoms of intoxication, nausea and vomiting. Abdominal pain. Sudden imperative feel-ing of defecation ends with a loud passage of flatus and spitting stool. Stool is liquid, watery, bulky and frothy, with a pungent odor, up to 5-15 times a day. The rotavirus is more common. V

iral

dia

rrh

ea

The disease is common in infants. It is accompanied by prolonged fever, severe intoxication. Stool is liquid, yellow-green color, with mucus and fetid odor. Symptoms of dehydration develop rapidly. The liver and spleen are enlarged.

Sal

mon

ello

sis

of

ente

riti

c fo

rm

The body temperature is normal. There is moderate pain in epigastrium. Abdominal murmur. Stool is liquid, watery, without mucus and blood, mixed with undigested food. Giardia are detected in the feces. G

iard

iasi

s

The body temperature increases to 38oC. Cramping abdominal pain. Stool is loose, liq-uid with mucus, bulky, watery, bright-yellow color. The anus is closed. There is an irritation around the anus and on the buttocks. It occurs in children under 1 year.

Col

i-in

fect

ion

Body temperature increases to 38-39oC. Stool is loose with mucus and blood; abdominal pain is cramping. The abdomen is sunken, spasm of sigma. Tenesmus. "Rectal spit." There are sphincteritis and compliance of the

Dys

ente

ry

anus.

45

DIAGNOSTIC ALGORITHMS : INTESTINAL COLI INFECTION

Affected organs

and systems

Clinical

syndromes

Signs and

symptoms

Form 46

Diagnostics

The differential

diagnosis

Treatment

Course of disease

Prophylaxis

Intestinal coli infection in infants

Gastrointestinal tractCentral nervous

systemCardiovascular system Liver Kidneys Metabolism

Enteritic Toxicosis Hypovolemic shock Exsicosis Hypokalemia

Liquid watery stools, flatulence

Atony, adynamia, persistent vomiting, anorexia, prolonged

fever

Pallor of skin, cyanosis of the lips,

acrocyanosis, tachycardia, pastosity

of skin structure, hypotony

Enlargement of the liver

Oliguria, anuriaExcitation, thirst, xerosis and skin

driness, weight loss

Sleepiness, heart sounds muffled,

muscular hypotonia, changes in the electro cardiogram, paresis of

the intestine

Serological examination

Radio-immunodiffusion

Bacteriological examination of stool

Luminescent-serological studies

Syndrome of impaired intestinal absorption

Simple dyspepsia Toxic dyspepsia Dysentery SalmonellosisStaphylococcal

enterocolitisCholera

Diet therapy Antibiotic therapyDetoxification and

rehydrationStimulating and vitamin therapy

Symptomatic Biopreparations

Acute Prolonged

Sanitary-hygienic regimen

Slight Moderately Severe Coli-sepsis Bacteriologic agent

Terminal disinfectionBacteriological

examination of contactExpedited reportIsolation of the patient

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF SALMONELLOSIS

Yes No Syndrome of gastroenterocolitic

intoxication.

Acute onset of the disease with rising of body temperature to 37.5-38-39oC. Vomit is abundant, mixed with food, and then watery, with flakes of mucus. Loose stook is up to 5-15 times a day, watery, bulky, yellow or yellow-green, frothy, with a bad smell, spitting. Sometimes it is a muddy whitish or pityriasis. Cramping pain is in the upper abdomen or umbilical region. The mucous membrane of the soft palate, small tongue, palatine arches partially hyperemic and slightly swollen, grainity is found. The liver and spleen are not enlarged.

Rot

avir

us

gast

roen

teri

tis

Acute onset of the disease, with occurrence of liquid stools,colorless, watery and bulky with floating flakes, like “rice water”, with no specific smell, mixed with mucus and blood, up to 3-10 times a day. Vomiting starts later than diarrhea. Temperature is reduced or subferile. There may be imperative feeling of defecation

Ch

oler

a

at night.

Acute onset of the disease with fever, nausea, repeated vomiting. Sometimes the temperature rises to 38-39°C. Cramp-like pain is in abdo-men, usually in the epigastric region. Stool be-comes loose, watery, with no significant patho-logical impurities, often green, frothy, with ad-mixtures of mucus and blood, with a sharp pu-trefactive odor. Tongue is coated, wet. The liver and spleen were not enlarged.

Inte

stin

al

pro

teu

s in

fect

ion

Acute onset of the disease. Regurgitation, vomiting, stop of weight gain and diarrhea are typical. Stool becomes more frequent up to 5-8 times a day. Stool is not formed, liquid, yellow-green with mucus and white lumps, with an unpleasant odor. There is a fecal stream during expressed aerogenesis. There is skin irritation around the anus.

Sim

ple

dys

pep

sia

Acute onset of the disease, with a rise of body temperature, headache, chills, pain in the abdomen. Stool is loose, bulky, slimy, with a pungent odor, as a "swampy slime." From the first days there are catarrhal signs, hyperemia of face, injection of scleral vessels, roseolous or maculopapular rash. The liver and spleen are enlarged.

Par

atyp

hoi

d А

, В

Acute onset of the disease with fever. Stool is about 10-15 times a day, watery, yellow or orange color, with an admixture of small amounts of mucus, without blood. The abdomen is moderately distended; soft, abdominal murmur is along the small intestine. The liver and spleen are not enlarged. The anus is closed, there is irritation around it and on the buttocks. Vomiting is persistent, but not often, 2-3 times a day. Regurgitation is typical. E

sch

eric

hio

sis

ente

rop

ath

ogen

icfo

rm

It is more common in infants. The disease develops gradually. The stool becomes bulky, loose, sometimes frothy, with white lumps, and sour smell. There are regurgitations, meteorism, murmur in the parts of the alimentary tract, steatorrhea, weight loss, diarrhea with putrid fermentation. Symptoms of D

ysb

acte

rios

is

..

polyhypovitaminosis. Acute onset of the disease with a rise of body temperature up to 38 - 39oС. Marked symptoms of intoxication. Nausea, repeated vomiting and abdominal pain. Frequent stool, from 2-3 to 15 times a day, often with mucus and blood. The abdomen is moderately distended. Sometimes the liver and spleen are enlarged. Sometimes there are catarrhal signs, in some cases - polymorphic eruption on the skin around the joints, on the hands, and feet.

Inte

stin

al

yers

inio

sis

Acute onset of the disease starts acutely, characterized by the gradual development and intensification of symptoms in 3-4 days. A stool from the first day of the disease has a significant amount of mucus, blood, has a dark green color; it becomes frothy, like "swampy slime." Vomiting is not common, but persistent. The body temperature rises from the 1st day of illness, reaching a peak in the first 3 days and lasts an average of 5-7 days. There is enlargement of the liver and spleen. S

alm

onel

losi

s

The disease is detected either after the introducing of complementary foods, or after the introducing of milk and manifests by persistent diarrhea, abdominal distention, vomiting, regurgitation, that leads to hypothrophy. Symptoms disapear after the elimination of intolerate food. There is no i

Syn

dro

me

of

mal

abso

rpti

on

ntoxication. The respond to therapy is poor.

43

DIAGNOSTIC ALGORITHMS : SALMONELLOSIS

Affected organs

and systems

Signs and

symptoms

Clinical

variants

Especially in children

1 year of age 44

Diagnostics

Differential

diagnosis

Flow

Treatment

Prophylaxis

SALMONELLOSIS

Gastrointestinal tract

Central nervous system

Cardiovascular system

Metabolism Liver Kidneys Spleen

Abd

omin

al p

ain,

per

sist

ent r

epea

ted

vom

itin

g, lo

ose

stoo

ls w

ith

muc

us,

bloo

d an

d gr

een,

coa

ted

tong

ue,

dist

enti

on, i

ndur

atio

n an

d te

nder

ness

of

the

colo

n

Feve

r du

ring

3-5

day

s,

flac

cidi

ty, w

eakn

ess,

an

orex

ia, c

oma,

co

nvul

sion

s

Sudd

en p

allo

r of

the

skin

, ta

chyc

ardi

a, m

uffl

ed h

ear t

soun

ds, d

ecre

ased

blo

od

pres

sure

Thi

rst,

dry

muc

ous

mem

bran

es a

nd s

kin,

w

eigh

t los

s

Enl

arge

men

t of

the

live

r,

jaun

dice

Oli

guri

a

Sple

nom

egal

y

GastricGastroenterological

EntericalGastroenterocolitic

EnterocoliticColitic

Toxico-septicalTyphoid Flu-like

ObliteratedTransient bacteriocarriers

Dyspeptic formsHigher frequency of

severe forms

Toxic-septical forms are more

common

NonpercutaneousToxicosis with

exsicosisProlonged carrying

Serologic studiesHematological

studiesCoprological examination

Bacteriological studies of feces,

vomit, blood, bile, urine

CholeraStaphylococcal enterocolitis

INTESTINAL coli infection

Dyspepsia Dysentery Viral diarrheaSyndrome of

malabsorption Typhoid fever

Chronic ProlongedAcute

Detoxificating diet, rehydration

Antibacterial Desensitization Stimulating Vitamins Biopreparations Symptomatic

Supervision of the work of nutrition

department Expedited report


Terminal desinfection

Examination of the contact


Dispensary of recovered

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF CHOLERA

Yes No

Watery diarrhea, vomiting, exicсosis

Acute onset of a triad of symptoms: rising of body temperature, vomiting and diarrhea. Vomiting precedes diarrhea, repeated, lasts - 1-2 days. The number of bowel movements/ defecation - from 10 to 15 times a day. Stool is loose, yellow, without any pathologic additives, sometimes discolored or turbid pale. Dura-tion of diarrhea is 3-6 days. Rotavirus is detected by electron microscopy.

Acute onset of a triad of symptoms: the rising of temperature of the body, vomiting and diarrhea.

It begins with the appearance of vomiting and diarrhea. Slight low-grade fever. Diarrhea lasts a day, up to 10 times a day, vomiting is not profuse. From the first day, there are signs of paralytic syndrome – vision disorders, dry mouth/ xerostomia. Xerostomia is noted at early stages in all pa-tients.

Rot

avir

al

gast

roen

teri

tis

Ocular symptoms are mydriasis, unresponsive pupils, aniso-coria, ptosis and diplopia. Paresis of the facial muscles/ facial mioparesis, dysphagia - patient feels “a lump in the throat”.

Bot

uli

sm

Paresis, paralysis of skeletal muscle. Botulinum toxin de-tected in biomaterials, taken from a patient Acute onset of disease. Feces are watery, yellow

or orange in color, with an admixture of a small amount of clear mucus, bulky, unformed “porridge-like”/ "wa-ter-gruel" – excrements are mixed with water, spitting, diapers are entirely moisten with them. After liquid absorption, mucus disappears and stool often seems normal. Vomiting 1-2 times a day. The rapid development of toxicosis with exicсosis. Bacteriological confirmation/verification of the diagnosis is the growth of the colonies E. Coli

En

tero

pat

hog

enic

es

cher

ich

iosi

s

Acute onset of disease. Regurgitations, stopping of the weight gain and diarrhea are noted. Loose stool is up to 5-8 times a day. Consistence of the fecal matters is not ho-mogenous, liquid, yellow green colored, with admixtures of mucus and white flecks with bad smell. Meteorism pro-vokes streaming of the excrements during defecation. There is an irritation around anus. Offensive breath, abdominal distention, coated tongue. There is no fever. There are die-tary variations in medical history/ personal history. A

cute

dys

pep

sia

Acute onset of disease, with pain in upper ab-domen, repeated vomiting, the temperature rising to 38-40 C, general weakness. Tongue is thickly coated, dry. The abdomen is moderately distended. Stool is up to 5 times a day, porridge-like or liquid, bulky, undigested, sometimes watery or frothy, with a significant amount of spinach color like “pond scum”, foul-smelling. Develop-ing of symptoms of toxicosis and exsicosis is gradual. Salmonella is found in feces, vomit mass and other sub-stances. Increasing of salmonella antibodies level in the patient’s blood.

Guiding symptoms are abdominal and dyspeptic. Pain is moderate, localized in anticardium, around the um-bilical region. Appetite disorders, nausea, unstable stool, up to 3-4 times a day. Stool with moderate amount of mucus, without blood, with admixtures of indigested food. Loss of appetite, asthenia. Diagnosis is based on finding/detecting of cyst or vegetative form of parasite in direct smear of fe-ces.

Sal

mon

ello

sis

(gas

troe

nte

riti

ssy

nd

rom

e)

Gia

rdia

sis

Acute onset of disease with the evaluation of the temperature of the body to 38-39°C. Symptoms of intoxi-cation are manifested. Nausea, vomiting, abdominal pain. Stool is from 2-3 to 15 times a day, often with admixtures of mucus, blood. Abdomen is moderately distended. The liver and spleen are enlarged. There may be catarrhal symptoms, polymorphous eruption on the skin around the joints, on the hands and feet. Diagnosis is based on Yer-sinia detecting in patient’s biological media/ discharges.

Inte

stin

al

yers

inio

sis

The course of disease is severe and causes high mortality rate. It begins suddenly, often at night. There is severe lancinating abdominal pain (colic), uncontrollable vomiting/anacatharsis/hyperemesis, watery diarrhea. There may be admixtures of mucus, sometimes blood. Dehydration develops rapidly. Short-term remission lasts 1-2 days, but after 2-3 days patient may die. Patient is in consciousness/alert/ up to agonal/moribund state/period. consciousness to preserve agonalnog period. In patient’s personal history - fact of the agarics eating, seasonality.

Dea

th c

up

mus

hro

om (

Am

anita

ph

allo

ides

)po

ison

ing

Acute onset of disease, with increasing the tempera-

ture of the body up to 38-39°C. Headache. Abdominal pain is cramping without distinctive localization. Stool is loose, becomes watery/ liquid, with admixtures of mucus and blood. At first day, feces are formed, after 2-3 days feces mass disappear completely, stool becomes mucous as like as “rectal spitting”, scanty, with blood streaks. Tenesmus and compliances of the anus.

Acute onset of disease, temperature of the body is normal. Diarrhea starts suddenly, often at night. Defeca-tion urge is painless, there isn’t abdominal pain. At first hours, feces are formed, then - watery, bulky, turbid white, with floating flakes like “rice-water”. There aren’t pathological admixtures. Acute/severe/ sharp weakness develops, adynamia. Bulky repeated vomiting without nausea. Vomit mass like to “meat slops”. Conditions of dehydration, hypokalaemia and oliguria make rapid pro-gress. Identification of cholera vibrio/ Koch’s bacillus is based on microscopic investigations of patient’s biologi-cal media/ discharges/

Dys

ente

ry

Ch

oler

a

41

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ALGORITHMS DIAGNOSTIC OF CHOLERA

Etiology

seasonality

Transmission mechanism

Affected

organs and systems

Clinical

syndromes

Clinical

symptoms

Clinical

forms

Methods of

diagnosis

Differential

diagnosis

Treatment

Clinical course

Prophylaxis

CHOLERA

GikoshimaInaba

Gastrointestinal tract Central nervous system

Cardiovascular

system Metabolism

Gastroenteritic Toxicosis with exicosis

Hypovolemic shock Hypokaliemia

Mild Medium-heavy

/severeSevere Algid state Atypical

Bacteriological of fecal culture, vomit

Luminescent-serological

Serologic methods

Escherichiosis Salmonellosis Viral diarrhea Mushroom poisoningToxicity of chemical

poisons

Antibiotics Vitamin therapy Symptomatic therapy

Alimentary

El-Tor

Summer

Ogawa

Contact-householdWater

Kidneys

Pro

fuse

vom

itin

g, w

ater

y st

ool,

abun

dant

wit

h m

uddy

-

whi

te f

lake

s fl

oati

ng r

emin

isce

nt o

f "r

ice

wat

er"

stoo

l fr

eque

ncy

3-10

tim

es a

day

and

mor

e

Hoa

rsen

ess,

low

er b

lood

pre

ssur

e, d

ry s

kin,

sev

ere

wea

knes

s, w

eakn

ess,

diz

zine

ss, h

ypot

herm

ia, t

hirs

t, w

eigh

t los

s, c

onvu

lsio

ns, m

uscl

e w

eakn

ess

Tac

hyca

rdia

, hyp

oten

sion

, cya

nosi

s of

the

naso

labi

al

tria

ngle

, acr

ocya

nosi

s

Oli

guri

a, a

nuri

a

Mus

cula

r hy

poto

nia,

dro

wsi

ness

, rap

id h

eart

sou

nds

muf

fled

obliteratedHaemorrhagicSubclinical Hypertoxic and «dry

cholera»

Disintoxication therapy

Intravenous rehydration

Fulminant With several layers of complications

Acute onset of a diseases


Terminal disinfection Bacteriological examination of contact

Dispensary observation of

recovered


Alarm (emergency notification)

42

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF TYPHOID FEVER

Yes No Intoxication. Syndrome of rash.

Generalized lymphadenopathy.

Low grade fever, weakness, distress. There is punctate rash on extensor surfaces of the joints, derierre, abdomen, the hips, without any changes on the skin. Catarrhal signs of the upper respiratory tract occur at the same time with the rash. The occipital lymph nodes are enlarged. CBC: leuco-penia, lymphocytosis, plasmacytosis.

In the medical history - contact with tubercu-lous patients, the errors of BCG vaccination. Disease develops gradually, long-term of low-grade fever, night sweats, loss of appetite. A slight enlargement of intermediate glands, failure to body weight gain, a tendency to intercurrent diseases. A slightly increased ESR, eosinophilia, lymphopenia. Bacteriologic ex-amination. Mantoux test. Chest roentgenography.

Ru

bel

la

tub

ercu

losi

s

Expressed catarrhal period: purulent discharge

from the nose, conjuctivitis, cough. Filatov - Koplik spots. There are menocelis and papular eruption phases. Period of rash is followed by a period of pigmentation, then defurfliration (defurfuration). CBC: leukopenia. M

easl

es

The course of disease is prolonged (for months). The tem-perature curve has the undulating nature. Hyperplasia of lymph nodes of all groups: lymph nodes are enlarged to the V-VII sizes, they are dense, matted together, and they aren’t freely movable. Lymph node biopsy reveals mirror-image cells/Sternberg cells

Lim

fogr

anu

lo-

mat

oz

Fever, the symptoms of respiratory catarrh, hyperplasia of lymphoid/adenoid tissue of oropharyngeal cavity. Cervical lymphadenopathy. Blenosis of the eyes: blennophthalmia/ The sharp/acute skin pallor, marked angiostaxis/

bleeding, enlarged spleen. The number of red blood cells and hemoglobin is reduced, accelerated ECR (erythrocytes sedimentation rate). Results of sternal puncture: increasing of myelocaryocytes, reducing of megakaryocytosis, myelopoiesis disorders. The amount of blast elements is sharply increased; the number of intermediate progenitor and mature forms of the cells of myeloid lineage is reducing.

catarrhal conjunctivitis, follicular conjunctivitis, membranous conjunctivitis. There are no changes in CBC.

Ad

enov

iral

in

fect

iou

s

acu

te le

uk

emia

Expressed intoxication. Punctuate scarlet fever rash. The rash appears on the hyperemic skin, on the 2nd day of the disease. Pallor of nasolabial triangle, resistant white autographism (dermographism). Intensity of natural folds. Pastia’s simptom. "Burning" mouth - limited hy-peremia of oropharynx. Strawberry tongue. Changing of phases of vegetative nervous system.

Sca

rlet

fev

er

Prolonged low-grade fever, lymphadenopathy, the liver and the spleen are enlarged. Sharp muscle pain, generalized arthralgia without visible changes in the joints. Chorioretinitis, progressive myopia. Changes in the autonomic nervous system. X-ray test reveals calcifications in the brain. Serological examination reveals growth of Toxoplasma antibody titer.

toxo

pla

smos

is

Florid symptoms of intoxication. Long duration. Pharyngoscopy reveals changes of necrotic tonsillitis (Henoch's angina in the throat). Hepatosplenomegaly. Ocu-loglandular form - purulent conjunctivitis. There are mono-nuclear changes (shifts in the blood). Thrombocytopenia, hematolysis (decreasing of blood coagulability). Serological examinations reveal increasing antibody titer. L

iste

rios

is

Acute onset, herpetic eruption on the lips. Abdominal pain, gaseous distention, diarrheal syndrome, borborygmus in the ileocecal region, nausea, and vomiting. Catarrhal signs of upper respiratory tract. Hepatosplenomegaly. Exanthema. The results of Widal test (Widal reaction) are negative. Studying of blood cultures and serologic exami-nations indicate the presence of specific antibodies.

Par

atyp

hoid

A a

nd

B

Fever, expressed catarrhal signs of the upper respiratory tract, the manifestations of diffuse bronchitis. Anorexia, dyspepsia, colitis, significant enlargement of the liver and the spleen. Slow regress of the symptoms. Hypochromic anaemia. A significant increasing of ESR, leukocytosis is more common. Abdominal pain. Causative agents are revealed by blood, bone marrow, feces, and bile examinations. Serological method/ antibody-mediated method: Wright-test shows increasing of antibody titer to 1:100.

bru

cell

osis

Prolonged fever, headache. Specific toxicity - somnolentia, hallucinations, deliration, loss of consciousness. The skin is pale and dry. Typhoid maculopapular rash on the skin of the abdomen. The middle of the tongue is coated with thick brown plaque, the tip and sides are clean, red. There are teeth indentations. Diarrhea syndrome - pea soup stools is up to 8-10 times a day. There is no nausea or vomiting. Hepatosplenomegaly. Widal reaction.

Prolonged low-grade fever, undue fatiguability, lymphoadenopathy, weight loss, obstructive cough without reversal, diarrhea syndrome. Upper gastrointestinal events with Candida (there is an oral and oesophageal candidiasis).

T

yph

oid

fev

er

Pneumocystic pneumonia. Dysfunction of the central nervous system (injury of the central nervous system). Kaposi's varicelliform eruption. Reducing number of T4

TAID

S

lymphocytes.

55

Diagnostic algorithms: typhoid fever

Affected organs

Signs and

symptoms

Characteristics in

children of early

age

Complications

Methods

of diagnostics

Differential

diagnosis

Principles

of treatment

Epidemiological features

Typhoid fever

Central nervous system

Gastrointestinal tract

Cardiovascular system

Skin Blood Other organs

Feve

r, v

omit

ing,

hea

dach

e, d

elir

ium

, co

nfus

iona

l sta

te, h

allu

cina

tion

s, f

oot c

lonu

s

Ano

rexi

a, c

onst

ipat

ion

or d

iarr

hea,

blo

atin

g,a

Pada

lka'

s sy

mpt

om, c

oate

d to

ngue

Bra

dyca

rdia

, voi

cele

ss to

ne, d

icro

tic p

ulse

Dry

ski

n, F

illi

povi

ch's

sym

ptom

, ros

eola

Ney

trof

ille

sis,

incr

ease

d er

ythr

ocyt

e se

dim

enta

tion

rat

e, le

ukop

enia

Bil

e du

ct, e

nlar

ged

live

r, e

nlar

ged

sple

en

Acute onset, shortening of the period of the clinical disease, repeated vomiting, toxicosis with exsicosis, the early appearance of roseola (may be absent), dyspepsia, tachycardia, leukocytosis

Hemorrhage Rare perforation

PneumoniaParotitisStomatitisEncephalitis CholecystitisMeningitis

Urine cultureIndirect

hemagglutination test

Widal's reaction

Stool cultureBlood culture

ARDEnterovirus

infectionSalmonellosisMeningitis

Miliary tuberculosis

LeukosisDysentery

Diet Skin and

mucous careBed regimen

Etiotropic therapy

Pathogenetic and

symptomatic

Bacteria carrying control

Dispensary observation reconvalesce

nce

Antiepidemic measures

Early diagnosis


Active immunisation

Rules of personal and

public hygiene

Sanitary and educational

activities

56

53

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSTICS OF VIRAL DIARRHEA

The syndrome of watery diarrhea

Hepatosplenomegaly, abdominal distension, abdominal pain (epigastric or generalized abdominal), a stool as a "spinach" or "frogspawn", persistent vomiting, long-term intoxication (up to 7 days).

Yes No

Sal

mon

ello

sis

At first there is diarrhea after that vomiting, dehydration, frequent stools (without counting) in form of rice-water and odorless. It occurs mostly in young children with rapid onset and elevation of body temperature.

Retraction of the abdomen, vomiting, spasmodic abdominal pain, spasm of the sigmoid colon, blood-streaked stool with mucus, "rectal" spit. Compliance of the anus.

Dys

ente

ry

Ocular symptoms join. Diarrhea is withoutpathological impurities, nausea and vomiting. In severe forms of respiratorydisorders there are pareses of the tongue muscles, soft palate and myasthenia. Pale skin, dullness of heart sounds, systolic murmur.

The disease occurs predominantly in children of the 1 year of life. Acute onset with the gradual development of symptoms, temperature is long and wavy; vomiting is infrequent, but prolonged; dis-tention, rumbling along the small and large intestines; bright yellow enteral stool. Dehydration symptoms develop often.

Col

ibac

illo

sis,

en

tero

pat

hoge

nic

for

m

Abdominal pain (in the intestine more in the ileocecal region), distention, borborygmus, loose stool with harsh odor which is profuse and slimy. Polymorphous eruption (roseolous, maculopapular, papular-roseolous).

Cho

lera

B

otu

lism

Par

atyp

hoid

Nausea, repeated vomiting 1-2 times a day, abdominal pain is spasmodic localized around the umbilicus or in the right iliac region. Borborygmus, diffuse tenderness along the small in-testine, ileum and caecum. Loose watery stool with mucus and greens and sometimes blood.

Inte

stin

al y

ersi

nio

sis

It occurs mainly in infants. Short vomiting,loose stools with yellow mucus, with whitish flecks (calcium soaps), sour smell.Elevation of body temperature. Diet leads to normalization of the state.

Sim

ple

dys

pep

sia

Mushroom poisoning often happens in August. There is sudden severe cutting pain in the abdomen, uncontrollable vomiting. Very frequent watery stools may be withmucus, sometimes blood. There is eatingmushrooms in the anamnesis.

Poi

son

ing

by

aman

ita

Contact with toxic chemicals, repeated vomiting and loose stool with mucus of fecal character. Pain is sharp, constant orspasmodic of cutting character in the abdomen. Impairment of consciousness may appear.

Poi

son

ing

by p

oiso

ns

Vomiting:initially with contaminant of food, then watery with mucus. Stool is watery, profuse, of yellow color with harsh odor. Stool may be muddy whitish or pityroid. Pain in the epigastric or umbilical region has permanent nature. It is characterized by imperative desire for stool accompanied by borborygmus and ends with loud discharge of gases and splash-stool.

TRot

avir

aql i

nfe

ctio

n

Diagnostic algorithms : viral diarrhea

Etiology

Seasonality

Forms

Characteristic

of forms

Course

Differential

diagnosis

Methods

of diagnostics

Features in children

up to one year

Principles of treatment

Prophylaxis

Viral diarrheas

Coronaviruses Calce virusesAdenoidal

virusesRotaviruses Cholera vibrio Reoviruses

Winter-spring

Typical Atypical

Easy Medium severe Severe Obliterated Asymptomatic

Tem

pera

ture

is u

p to

37,

vom

itin

g is

sev

eral

ti

mes

a d

ay, t

he li

quid

gru

el s

tool

is

2–5

tim

es a

day

Tem

pera

ture

is f

ebri

le, v

omit

ing

is

repe

ated

or

mul

tipl

e, p

ale

skin

, thi

rst,

stoo

l 8–1

6 ti

mes

Sto

ol 2

5–30

tim

es, d

ehyd

rati

on o

f th

e I

I–II

I de

gree

wit

h ex

icco

sis,

rep

eate

d vo

mit

ing,

ta

chyc

ardi

a, d

eafe

n of

the

hea

rt s

ound

s

Man

ifes

tati

ons

are

mil

d, s

hort

-ter

m c

ours

e,

reve

aled

in th

e ex

amin

atio

n of

the

cont

act

chil

dren

wit

h fo

cus

Com

plet

e ab

senc

e of

man

ifes

t sym

ptom

s,

rota

viru

s is

fou

nd in

the

chil

d , t

he

imm

unol

ogic

al s

hift

is d

eter

min

ed

Lingering With

complications Mixed infectionAcute

ShigellosisSimple

dyspepsiaSalmonellosis Colibacillosis Cholera

Virological

Specific immunological tests: indirect hemagglutination test

(IHGT), immunofluorescence test (IFT), ELISA, RIA

Rare, sometimes sporadic or group outbreaks in maternity

hospitals

More common in children of 6-12

months

Rotavirus gastroenteritis in a

form of mixed infection

It proceeds hardly through dehydration and complications

Secondary lactase deficiency is

formed

Bioremediesenzymes

Antidiarrheal remedies

Antiviral immunoglobulinDiet therapy

Rehydrationdesintoxication

Sanitary-educational work Disinfection

Following up of contact

personsFinding out isolation of

patients

Maintain of personal and public hygiene

Bacteriological

Summer

Phagotherapy of contacts

54

49

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF DYSBACTERIOSIS

Syndrome of diarrhea. Intoxication.

Hepatosplenomegaly, abdominal distension, abdominal pain (epigastric or around the abdomen), stool as "swamp slime" or "frogspawn", persistent vomiting, long-term intoxication (up to 7 days).

Yes No

Sal

mon

ello

sis

Diarrhea and then vomiting, dehydration, frequent stools (times out of number) in the form of rice-water and odorless. It is the most common in young children, with rapid onset and increase of body temperature to high numbers.

Retraction of the abdomen, vomiting, cramping abdominal pain, spasm of the sigmoid colon, stools with mucus, bloodstreaks, "rectal" spit. Compliance of the anus.

Dys

ente

ry 1. Neuroparalytic syndrome: visual impair-

ment, dry mouth, dilated pupils with a reduction or even nonreactive for the light, convergence and accommodation.Sometimes anisocoria, paralysis of accommodation may occur. The «netting»appears before the eyes. Ptosis, diplopia. 2. Paresis of the facial muscles, resulting inamimia, masklike face. Dysphagia. Thenparesis and paralysis of skeletal muscles of the trunk and extremities manifest.

It occurs predominantly in children younger than 1 year old. Acute onset with gradual development of symptoms, long, wavy temperature, infrequent, but prolonged vomiting, bloating, abdominal sounds along the small and large intestines; enteritis stool of bright yellow color, symptoms of dehydration often develop.

Col

ibac

illo

sis,

en

tero

path

ogen

ic f

orm

Children suffer from it more often than adults. It starts acutely; stool is profuse, liquid and watery, without any admixtures of mucus and blood, of dull whitish color. Vomiting is rare. Abdomen sounds are loud. The urge to defecate has an imperative character. Renal failure, acidosis. Dehydration. The pain is in the epigastrium and umbilical region. During winters.

Ch

oler

a B

otu

lism

Rot

avir

al in

fect

ion

The disease is more common in young children. It develops gradually. The stool becomes profuse, liquid, sometimes with white foamy flecks, sour smell. Posseting, meteorism, abdomen sounds in various parts, steatorrhea, weight loss, diarrhea with putrid fermentation often occur. Symptoms of polyhypovitaminosis.

Dys

bact

erio

sis

It occurs in infants and is associated usuallywith the introduction of feeding up, or transfer the child to bottle feeding. In these cases, the rapid introduction of supplementary food is not appropriate for the quality or quantity of food of the child's age, leads to functional impairment of the intestine. No intoxication, posseting. A child is relatively calm. Stool is softening, without pathological impurities. After the elimination of the nutritive cause alldisorders rapidly disappear.

Sim

ple

dys

pep

sia

The stool includes increased amounts offats. It is bulky and porous, grayish, occasionally becomes liquid, watery.Multiple stool. Loss of weight, big belly.Extended and elongated colon, which remains the same after the disappearance ofthe main symptoms. C

elia

c d

isea

se

The disease begins in newborns since birth. Belly is big, intractable, stable constipation. Subcutaneous veins are dilated, umbilicus is protruded. The child is pale, emaciated, arms and legs are disproportionate. The child stunts from peers. Digital anus examination gives a sense of increased sphincter tone of the rectum. T T T T T T

Meg

acol

on

http://www.multitran.ru/c/m.exe?t=325351_1_2&s1=%FD%F8%E5%F0%E8%F5%E8%EE%E7

Diagnostic algorithms: intestinal dysbacteriosis

Causes

Clinlcal

forms

Signs and

symptoms

Characteristics

in different

age groups

Methods

of diagnosis

Differential

diagnosis

Treatment

Preventive measures

Intestinal dysbacteriosis

Irrational use of antibiotics

Abnormal feeding

Presence of chronic foci of infection

Appointment of immunosuppres

sants

Radiation therapy

Malabsorption syndrome

Intestinal underdevelo

pment

Factors that reduce the

body's resistance

Compensated Subcompensated Decompensated

Baby looks healthy, normal stools, good appetite, body weight is

added gradually, disturbed intestinal microflora

Clinical symptoms are moderate, slack, pooreater, poor body weight gain, intestinal

disorders appear

Bad condition, evident intoxication, vomiting, loss of

appetite, decrease of body weight, loose stools

Disbacteriosis in young children Dysbiosis in older children

Posseting, poor weight gain, bloating, flatulence, borborygmus, steatorrhea, stool is liquid or gruel, foamy, with white lumps, profuse,

with a sour odor, undigested

Persistent usual constipation alternating with diarrhea, recurrent intestinal colic, dyskinesia of the gastrointestinal tract, belching, feeling of fullness, appetite is slightly decreased, undigested

stools

Study of stool microflora The immunological analysis

1 degree —anaerobi

c flora prevails over the aerobic flora,

opportunistic flora planted

104-102

2 degree — is an

anaerobic flora,

opportunistic

flora106–107

and replaced with atypical

variants

3 degree — dominated by aerobic

flora, opportunisti

c pathogenic

flora increases rapidly

Decrease in humoral and cellular indicators from moderate to severe

ones, depending on the degree

Diet depending on the child's age with the inclusion of preparations

with bifidobacteria

Enzyme preparations —abomin, pancreatin, festal,

smekta, mezim forte

Bifiсol, colibacterin, lactobacterin, bifidumbacterin, complex

immunodrugs, specific bacteriophages

Rational use of antibioticsRational nutrition with restriction of the use

of refined productsPrevention of intestinal infections

Opportunistic pathogenic acute intestinal infections

Acute bacterial and viral intestinal infections Nonspecific ulcerative colitis

50

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF INTESTINAL YERSINIOSIS

Yesд

No Diarrhea syndrome. Intoxication syndrome, rash.

Acute onset of the disease with fever up to 38oC. It happens most often in children younger than 2 years. Cough, runny nose, congestion of the mucous oropharynx appear. In 1-3 days pain in the abdomen and diarrhea for 5-10 times a day sometimes with mucus occur. Often there is repeated vomiting. There is the presence of multiform maculo-papular rash all over the body, and hyperemia of the body, especially of the face and neck.

The disease develops gradually. Stool is profuse

Dys

bac

teri

osis

, liquid, sometimes frothy with white

En

tero

viru

s

infe

ctio

n,

inte

stin

al f

orm

lumps. Frequent posseting, meteorism, abdominal sounds in the various parts, deficient body weight gain. There is no intoxication. The rash is absent.

Acute onset of the disease with fever up to 38-40oC, headache, chills, muscle and joint pain. Mild catarrhal signs. Nausea, vomiting, and epigastric pain. There is a loose stool 2-3 times a day enteritic-like. Rash outbreaks at once, and has either a punctate or maculosus character. It is located in the abdomen, in the axillary regions, on the lateral surfaces of the body, it is confluent around the large joints. P

seu

dot

ub

ercu

losi

s

The disease begins acutely; fever, vomiting, sore throat occur. In a few hours there is a punctate rash on unchanged skin, which spreads very rapidly on the face, neck, trunk and limbs. It is characterized by a bright localized from the hard palate hyperemia (catarrhal, follicular, necrotic tonsillitis). Diarrheal syndrome is absent.

Sca

rlet

fev

er

It begins acutely with a temperature rise to 38.5 - 39oC, upper respiratory catarrh and conjunctivitis appear. There are grayish-white spots on the buccal mucosa. Maculo-papular rash occurs in 4-5 days, which is manifested in three stages: 1 day - face, neck, 2 day - trunk, arms, 3 day - legs. Bowel disorders are not observed.

Mea

sles

The disease occurs in newborns, premature babies and infants. Acute onset of diseases, with the temperature rise. There are suppurative foci in various organs. It occurs on the background of frequent stool. Headache, vomiting, loss of appetite, bloat. Hepatosplenomegaly. Roseolous-papular rash is not

Sal

mon

ello

sis

of

sep

tic

form

Acute onset of the disease. There may be posset-ing, vomiting, deficient body weight gain, diar-rhea. Stool is more frequent up to 5-8 times a day. Consistency of feces is heterogeneous, liq-uid, slime green color, with mucus and white lumps, with an unpleasant odor. During aero-genesis stool is thrown like a jet. There is no temperature and rash.

Dys

pep

sia

severe.

Acute onset of the disease, headache, chills, pain in the abdomen. Bowel disorders, distension. From the earliest days there are catarrhal signs, hyperemia of face, injection of scleral vessels, conjunctivitis. At its height roseolous or maculopapular rash appears for several days. P

arat

yph

oid

A

Acute onset of the disease It starts acutely with short-term body temperature rise up to 38 -39oС. Symptoms of intoxication are marked. Nausea, repeated vomiting and abdominal pain. Stool is from 2-3 to 15 times a day often with mucus and blood. The abdomen is moderately distended. Sometimes the liver and spleen are enlarged. Sometimes there are catarrhal signs, in some cases there is polymorphous eruption on the skin around the joints, on the hands, feet.

Inte

stin

al

yers

inio

sis

Acute onset of the disease with temperature rise up to 38 -39oC that lasts at least for 3 days. Vomiting is single or repeated. Headache, pain in the abdomen. Stool quickens, it becomes liquid

Dys

ente

ry

, with mucus and blood. At first the stool has a fecal character, then in 2-3 day feces disappear completely, the stool becomes poor, so-called "Rectal" spit is a lump of mucus and blood. Tenesmus is marked. There is no rash.

47

DIAGNOSTIC ALGORITHMS: INTESTINAL YERSINIOSIS

Etiology

Seasonality

Mechanism of transfer

Affected organs

and systems

Clinical

forms

Course

Methods

of diagnosis

Differential

diagnosis

Principles

of treatment

Preventive measures

Intestinal yersiniosis

Iersinia enterocolitica

Winter-spring period

alimentaryaerogeniccontact-household

gastrointestinal tract

the respiratory system

Central nervous systems

livercardiovascular

systemjoints skin

gastrointerstinal pseudo-appendicular

septic erythematous hepatic articular

Into

xica

tion

, nau

sea,

vom

itin

g, f

latu

lenc

e,ab

dom

inal

pai

n in

the

ileo

ceca

lar

ea, d

iarr

hea

– pr

ofus

e w

ater

y st

ool w

ith

muc

us

and

gree

n, th

e sy

ndro

me

of e

nter

itis

and

gast

roen

teri

tis

Into

xica

tion

, vom

itin

g, a

nore

xia,

abd

omin

al p

ain

in th

e ri

ght i

liac

reg

ion,

dia

rrhe

a

Into

xica

tion

, wei

ght l

oss,

pro

long

edfe

bril

e fe

ver,

conv

ulsi

ons,

hep

atos

plen

omeg

aly,

ras

hon

the

skin

, a

rthr

itis

, abd

omin

al p

ain,

dia

rrhe

a, s

ever

e pa

llor

, dul

lnes

s of

hea

rt s

ound

s

Into

xica

tion

, pol

ymor

phou

s sk

in r

ash

arou

nd th

e jo

ints

on

the

hand

s an

d fe

et a

s p

ainf

ul p

ink

node

s w

ith

cyan

otic

ting

e

Into

xica

tion

, abd

omin

al p

ain,

he

pato

sple

nom

egal

y,ja

undi

ce, d

iarr

hea,

dar

k ur

ine,

dis

colo

red

stoo

l

Into

xica

tion

, art

hrit

is, s

wel

ling

, ten

dern

ess,

li

mit

atio

n of

mov

emen

t

relapsing

bacteriological culture of mucus from the

th t

the reaction of indirect hemagglutination

bacteriological culture of blood

bacteriological culture of urine

bacteriologic culture of feces

enzyme immunoassay

agglutination test

Shig

ello

sis

Ent

erov

irus

infe

ctio

ns

Salm

onel

losi

s

Typ

ho p

arat

hyph

oid

infe

ctio

n

Pse

udot

uber

culo

sis

Mea

sles

Rub

ella

Corticosteroids VitaminsNonsteroidal preparations

DesintoxicationAntibiotic treatment

Work in the focus with the contact

personsIsolation of patients

Early identification of sources of

infection

Sanitary and hygienic regime

Scar

let f

ever

Rhe

umat

ism

Sep

sis

Vir

us h

epat

itis

Acu

te a

bdom

en

Bru

cell

osis

Rehydration Antihistamines Diet

acute

48

31

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF PSEUDOTUBERCULOSIS

Yes No Punctate rash syndrome. Intoxication, catarrhal syndrome.

Catarrhal symptoms. Micropunctate rash is followed by peeling of the skin. Tachycardia, often vomiting. Bright redness of throat - "flaming" fauces. Lamellar skin flaking, especially on the fingers. Tonsillitis, lymphadenopathy, "strawberry" tongue. The rash does not leave the pigmentation. Pale nasolabial triangle. Rash is heavily on the cheeks, on the sides of the trunk, below abdomen, flexor surfaces of the extremities. The rash is on the hyperemic skin.

Sca

rlet

fev

er

Maculo-papular rash, large spotted rash, catarrhal symptoms, subfebrile temperature. Staging of rash on the hyperemic skin is typical. After the rash disappears, brown hyperpigmentation of the skin persists for several days. Filatov-Koplik’s spots, conjunctivitis. Sometimes croup syndrome, rash is prone to be confluent.

Mea

sles

Catarrhal signs. The rash is multiform, punctate, maculosis-papular, hemorrhagic, often around the joints, on the hands, feet (symptoms of "gloves" and "socks"). Joints inflammation (swelling, redness, tenderness and limitation of motion). Myocarditis. Hepatosplenomegaly. Nausea, vomiting, abdominal pain, heavy sweating, high fever with large daily scale, full-blown jaundice, diarrhea. Loose stool, often with mucus, green, sometimes with blood.

Inte

stin

al y

ersi

nio

sis

Body temperature is subfebrile. The rash is small maculosis, sometimes papular, not abundant, doesn’t leave pigmentation and desquamation after fading. It is not confluent. Rash hasn’t staging. Occipital and back cervical lymph nodes are swollen. Conjunctivitis is weak. In blood there is leukopenia, relative lymphocytosis, plasma cells (10-30%).

It begins acutely with temperature rise, symptoms of intoxication, abdominal pain, bloating, increased bowel sounds and pain along the intestine, in the ileocecal region. Catarrhal signs, hyperemia of face and injection of scleral vessels, conjunctivitis, herpetic eruption on the lips. Roseolous rash or maculo-papular rash, hepatosplenomegaly, sweating. In the blood there is normocytosis, neutrophilia, increased erythrocyte sedimentation rate. In severe cases complications are possible.

Par

atyp

hoi

d A

Menocelis, malaise, temperature rise, usually up to subfebrile, itchy skin, increased peripheral lymph nodes. Rash is confluent, it hasn’t any stages, it is associated with drug administration (often sulfanilamides, antibiotics, etc.). In the blood there is moderate eosinophilia. The rash is usually on the extensor surfaces. M

edic

amen

tal

der

mat

itis

Body temperature is increased, sometimes with the symptoms of intoxication. Joint pains, icteric sclerae, mucous membranes of the oropharynx, and then the skin. Aching pain is in the right hypohondrium, some person has itching. Hepatosplenomegaly. At the end of the preicteric period urine becomes dark and stool becomes discolored. Symptoms of dyspepsia occur. In the blood there is leukopenia, neutropenia, relative lympho-and monocytosis, increased direct bilirubin, thymol test is increased, prothrombin index is reduced.

Hep

atit

is A

Acute onset of the disease with fever, catarrhal signs. Lymphadenopathy - cervical, back cervical nodes, located behind sternocleidomastoid muscle by chain. Tonsillitis, hepatosplenomegaly. There are atypical mononuclear cells in blood. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase are increased. In the throat there are necrotic changes of tonsils. Plaque is not completely rubbed between the glass slides. It does not bleed when it is removed, can be easily removed. If you try to remove incrustations with tweezers they tear and crumble. Maculosis rash. In

fect

iou

s m

onon

ucl

eosi

s

Ru

bel

la

Acute onset of the disease, fever increases to 38-40oC, the symptoms of intoxication, muscle and joint pains, catarrhal signs. There are pains on swallowing, dizziness, nausea, vomiting, abdominal pain often in the right iliac region or in the epigastrium. Sometimes loose stool may be for 2-3 times a day. Puffiness and redness of face, neck, pale nasolabial triangle. Conjunctival hyperemia and vascular injection of sclera. Hyperemia of the pharynx, symptoms of "hood", "gloves", "socks." Micropunctate hyperemic rash occurs sometimes on unchanged skin. Skin itching. Localization is the abdomen, axillary regions, on the lateral surfaces of the body. Hepatosplenomegaly. TPse

ud

otu

ber

culo

sis

Acute onset of diseases, high fever up to 39oC and above. Rash is small maculo-papular. Headache, muscle pain, scleritis, catarrhal signs. Vomiting and abdominal pain may be often. Localization of the rash is on a face, body, sometimes on hands and feet. The rash is located on the background of unchanged skin. There is no staging, it does not leave pigmentation and desquamation.

En

tero

viru

s

(Bos

ton

exa

nth

ema)

Diagnostic algorithms : pseudotuberculosis

Etiology

Seasonality

Mechanism

of transmission

Affected organs

and systems

Clinical

forms

Clinical

symptoms

Methods

of diagnosis

Differential

diagnostics

Principles

of treatment

Course

Preventive measures

Pseudotuberculosis

Pseudotuberculosis bacteria

Winter-spring

Skin Joints LiverRespiratory system

Nau

sea,

vom

itin

g, a

bdom

inal

pai

n, b

owel

dis

orde

rs, d

ry

tong

ue c

oate

d w

ith

sabu

rra;

by

the

end

of th

e se

cond

wee

k of

illn

ess

ther

e is

a r

aspb

erry

tong

ue

Join

t pai

n, s

wol

len

join

ts, h

ot to

the

touc

h, m

ostl

y th

ey a

re

wri

st, e

lbow

, pha

lang

eal j

oint

s

Liv

er e

nlar

gem

ent,

tend

erne

ss o

n pa

lpat

ion,

icte

ric

scle

rae,

oc

hrod

erm

ia, d

ark

urin

e, in

blo

od c

onju

gate

d bi

liru

bin

frac

tion

is in

crea

sed

Com

bina

tion

of

sym

ptom

s

Sep

sis

Mal

aise

, sub

febr

ile

tem

pera

ture

, eph

emer

al r

ash

lesi

ons

of t

he o

rgan

s an

d sy

stem

s

Arthralgic Icteric Combined Generalised SepticAbdominal Suppressed SubclinicalScarlet

fever-like

Bacteriological Serological

Airborne- dust

Alimentary Droplet

Eyes Lymphatic

system

Gastro-intestinal

tract

Cardio-vascular system

Spleen

Catarrhal

Pun

ctat

e sc

arle

t fev

er r

ash

(ski

n on

the

ches

t, el

bow

, gro

in,

arm

pits

), w

hite

der

mog

raph

ism

, coa

rsel

y sp

otte

d pa

pula

r ra

sh (

on th

e fa

ce, n

asol

abia

l tri

angl

e; a

bdom

en, b

ack,

aro

und

the

join

ts),

pet

echi

al, h

emor

rhag

ic r

ash,

ery

them

a

No

clin

ical

sign

s, th

e di

agno

sis

is b

ased

on

labo

rato

ry te

sts

Cou

gh, r

unny

nos

e, s

ubfe

bril

e te

mpe

ratu

re, A

RV

IBlood

culture, culture of

feces, throat swabs

Serological reactions

Typhoid, paratyphoid

Measles Appendicitis Diarrhea HepatitisSepsisScarlet fever

Enteroviral disease

Rheumatism

Etiotropic: levomycetin

Nonsteroidalpreparations

AcuteUndulating course with

exacerbations and relapses

Proper storage of food

Bacteriological control of food products

The fight against rodents

Detoxification therapy syndromic treatment

32

29

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF VIRAL ENCEPHALITIS

Yes No Intoxication. Impaired consciousness. Convulsions. Focal symptoms.

Severe headache, especially in the fronto-temporal region, dizziness, pain in the abdomen, legs, and sometimes bleeding from the nose. Repeated vomiting, temperature is 38-40oC, impaired consciousness, sopor-comatose state, convulsions. Hyperemia of the face, chest. On the spot of the bite there is a local reaction - a little redness and infiltration of the underlying tissues with regional lymphadenitis. Enlargement of the liver, flaccid proximal paralysis or paresis of the upper limbs, the symptom of “sagging neck”, “Sprengel’s deformity”, meningeal symptoms. T

ick

bor

ne

ence

ph

alit

is It occurs usually in 7-9 days after vaccination at

high body temperature, at the height of the general and local reaction. Generalized tonoclonic spasms of varying duration - from a few seconds to several hours. Anxiety, shudder, motor automatisms, tremor of limbs, the recovery of reflexes or anisoreflexia, pyramidal signs. In older children there is a hallucinatory-delirious syndrome, psychosensorial disorder, cataleptic phenomena. CSF is not changed. E

nce

ph

alit

ic r

eact

ion

Intoxication, body temperature rise to 39-40oC, anxiety, repeated vomiting is not related to ingestion, it does not bring relief. Generalized convulsions, severe headache, dizziness, somnolentia, lethargy, hyperesthesia, positive meningeal symptoms, bulging of anterior fontanelle, position of "pointing dog", cranial nerves damage, vestibular disorders. Purulent: CSF is turbid, follows with rare drops, neutrophils predominate. Protein is increased, sugar is normal or reduced. Intracranial pressure is increased. Serous: CSFis clear, under the pressure. Initially cytosis is neutrophil-lymphocyte, then lymphocytic. Protein, sugar, chlorides usually do not elevated. Reaction is negative or weakly positive.

Ser

ous

and

pu

rule

nt

men

ingi

tis

Prolonged clinical course, prolonged fever, convulsive activity, hypertension-hydrocephalic syndrome. Child has problems with psychophysical development. Febrile reaction has the irregular wavy character. Often the secondary bacterial infection follows. Anxiety, poor sleep, weight loss, poor appetite, frequent posseting, fontanelle bulging, separation of cranial sutures, increasing of the head size. C

ytom

egal

ovir

al

ence

ph

alit

is

Acute onset of the disease, with body temperature rise, malaise, headache. Herpetic eruption appears on skin, gingivostomatitis is in the anamnesis. There are neurological symptoms. Impaired consciousness, moderate meningeal syndrome, rarely local clonic-tonic convulsions, repeated many times during the day. Hemiparesis and hemiplegia, amnesia, aphasia, neurosis-like syndrome and syndrome of liquor hypertension. There are the lesions of cranial nerves and motor oculi nerves. There is a herpes simplex virus isolated in the cerebrospinal fluid. Changes are typicalfor serous meningitis in CSF analyses.

Acu

te e

nce

ph

alit

is c

ause

d b

y h

erp

es s

imp

lex

viru

s

Loss of consciousness, nausea, vomiting, headache, cerebral symptoms. The disease manifests suddenly. Oculomotor disturbances (strabismus, "floating" eyeballs, abnormal pupillary response, size and shape of the pupils, the dissociation of reflexes, paresis of facial muscles, arterial hypertension, convulsive syndrome. C

ereb

rocr

ania

l tr

aum

a

Acute onset of the disease, with body temperature rise to 39-40oC. Chill, headache, nausea, vomiting, meningeal symptoms, scleritis, catarrhal conjunctivitis. Patients are obnubilate, indifferent, unresponsive to examination and surrounding. Rarer: excitement with delusions, hallucinations, loss of consciousness, muscle hypertension, which makes the patient lie with the throw back head and adducted towards the abdomen legs. Mono- or hemiparesis, flaccid paralysis, disturbance of breathing, swallowing, the fall of cardiovascular tone. Hyperkinesis of the facial muscles and upper limbs, sweating, and the lability of the cardiovascular system. In CBC: leukocytosis, neutrophilia, lymphopenia, eosinopenia, increased ESR. Lymphocytic cytosis, slight increase of protein.

Jap

anes

e en

cep

hal

itis

TE

pid

emic

(TTen

cep

hal

itle

thar

gic)

is

The disease is caused by injuries, aneurysms. Cerebrospinal fluid is bloody, during defecation there is a xanthosis. The pressure is 250-400 millimeter of water. Rate of fluid outflow is over 70 or like a jet. Cytosis is in the early days in accordance with red blood cells count, 5-7 days after it is 0,015-0,12. There is no sugar. Puncture brings considerable relief. S

ub

arac

hn

oid

al

hem

orrh

age

Motor excitement, impairment of consciousness, convulsions, leisure of nervous system. Flattening of the nasolabial folds, the deviation in the tongue direction, increased tendon reflexes, anizoreflexia, foot clonus, nystagmus, tremor, ataxia, light hyperkinesis, hemi-monoparesis, oculomotor disturbances. In younger children cerebral symptoms are expressed more clearly, they are often cerebellar.

TMen

ingo

ence

ph

alit

is

Catarrhal signs, body temperature rise, headache, chills, nausea, vomiting. Oropharynx is hyperemic, sleep disturbance occurs early. Patients are sleepy during the day and suffer from insomnia at night (inversion of sleep), oculomotor disturbances - ptosis, impaired convergence, diplopia, paralysis of accomodation, flac-cidity or loss of pupillary response. Face is masklike, mimic is sluggish. Vestibular disturbances are dizziness, unsteady gait, nystagmus. Vegetative disturbances are T

sweating,T Thypersalivation,T ThyperkinesisT. TIn CBC: moderate neutrophilicT Tleukocytosis, T Tincreased ESRT.

DIAGNOSTIC ALGORITHMS: VIRAL ENCEPHALITIS

Etiology

Clinical

syndroms

Clinical

symptoms

30

Methods

of diagnosis

Differential

diagnosis

Principles

of treatment

Complications

Viral encephalitis

Epidemic encephalitis

Epidemic parotitisCytomegalovirus

encephalitisMeasles

encephalitisChickenpox encephalitis

Rubella encephalitis

Postvaccinal encephalitis

Meningeal Encephalitic Paralytic Toxic

Tri

pod

sign

, hea

dach

e, n

eck

stif

fnes

s,

Ker

nig'

s si

gn, B

rudz

insk

y's

sym

ptom

Ocu

lom

otor

dis

turb

ance

s, s

yndr

ome

of

foca

l bra

in le

sion

s, h

yper

kine

sis,

sta

tic

and

loco

mot

or a

taxi

a, e

pile

ptif

orm

fit

s

Mon

opar

esis

, hem

ipar

esis

, fla

ccid

pa

raly

sis

Fev

er, d

yspe

ptic

dis

orde

rs, i

mpa

irm

ent

of c

onsc

ious

ness

Serological reactions, HGIR, lumbar puncture, virological and bacteriological study of CSF, the study of biological fluids (stool, throat swab, CSF), CBC, urinalysis, blood culture, studies of platelets, tuberculin tests, serum electrolytes, blood glucose, blood urea and blood creatinine, cranial X-ray, chest, X-ray,

EEG

Infections — meningitis of different etiologies, Rocky

Mountain spotted fever, brain abscess

Metabolic coma - Reye's syndrome, hepatic coma,

hypoglycemia, acute adrenal insufficiency, hypo-and hyperkalemia, uremia,

alkalosis and acidosis

Toxic coma - acute poisoning, salycylate

poisoning, lead encephalitis, nitrogen monoxide poisoning

Primary disease of the brain - the first attack of epilepsy,

posterior fossa tumors, cerebrovascular disease

Others - cerebral embolism, systemic angiitis,

postinfectious encephalopathy, trauma

("battered child" syndrome)

Antiinflammatory(glucocorticosteroid

therapy)

Dehydration Antihistaminic Vitamin therapy Symptomatic Antiparkinsonian Surgical treatment

Neurological disorders Psychotic disorders Mental deficience ParkinsonismPersistent

hyperkinesisEpileptiform attacks

Diencephalic disorders

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF VIRAL HEPATITIS

syndrome of jaundice

Cythemolytic icterus Hepatocellular jaundice Obstructive jaundice

Hereditary Acquired Infectious Noninfectious

Min

kow

ski-

Cha

uffa

rd’s

he

redi

tary

m

icro

sphe

rocy

tosi

s

Her

edit

ary

stom

acyt

osis

H

ered

itar

y he

mol

ytic

an

emia

cau

sed

by th

e de

fici

ency

of g

luco

se-6

-ph

osph

ate

dehy

drog

enas

e

T

hala

ssae

mia

A

utoi

mm

une

hem

olyt

ic a

nem

ia

P

arox

ysm

al n

octu

rnal

he

mog

lobi

nuri

a

Hep

atit

is A

Hep

atit

is B

Hep

atit

is C

Hepatic cirrhosis

fine

ly n

odul

ar

larg

e no

dula

r

bili

ary

Acu

te a

lcoh

olic

he

pati

tis

Dru

g-in

duce

d

hepa

titi

s

Cho

lest

atic

vi

ral h

epat

itis

Ja

undi

ce a

t tum

ors

jaun

dice

at

gall

ston

es

Jaun

dice

cau

sed

by p

aras

ites

(o

pist

horc

hias

is,

schi

stos

omia

sis,

clo

norc

hias

is)

In t

he c

lini

cal

find

ings

the

re i

s ja

undi

ce,

anem

ia,

enla

rgem

ent

of t

he s

plee

n.

THbT

Tdecr

ease

s to

eryt

hroc

ytes

40-

50 g

/ L

, bi

liru

bin

incr

ease

s (5

0-75

mcM

/ l

). T

he d

iam

eter

of

dec

reas

es,

and

the

thic

knes

s in

crea

ses.

The

for

m i

s sp

heri

cal.

The

con

-te

ntof

reti

culo

cyte

isin

crea

sed

TMar

ked

bili

rubi

ntw

o T Tcu

rved

line

s.

ane

mia

(70

-90

g / l

). E

nlar

gem

ent o

f th

e sp

leen

. Jau

ndic

e is

due

to in

dire

ct

. Def

ect i

n er

ythr

ocyt

e m

embr

ane

- co

lour

less

par

t of

the

cent

er is

lim

ited

by

TSig

nifi

cant

enl

arge

men

t of

live

r an

d sp

leen

acc

ompa

nied

by

jaun

dice

. The

incr

ease

of

Tbili

rubi

n is

Tanis

opoi

them

.

due

to th

e di

rect

fra

ctio

n. I

n th

e bl

ood

ther

e ar

e in

crea

sed

reti

culo

cyte

s,

kilo

cyto

sis,

"ta

rget

like

" er

ythr

ocyt

es a

nd m

ulti

ple

baso

phil

ic in

clus

ions

in

Jaun

dice

,ch

arac

ter

enla

rged

. Bil

irub

in is

40-

60 m

cMde

crea

sed.

sev

ere

wea

knes

s, a

rthr

algi

a, a

bdom

inal

pai

n, p

ain

in h

eart

, low

er b

ack

are

isti

c fe

atur

es T

empe

ratu

re o

f th

e bo

dy is

incr

easi

ng. T

he li

ver

and

sple

en a

re

/ l d

ue to

the

indi

rect

fra

ctio

n. H

emog

lobi

n is

T

he n

umbe

r of

ret

icul

ocyt

es is

incr

ease

d; m

acro

cyto

sis,

m

icro

sphe

rocy

tosi

s;os

mot

icre

sist

ance

ofer

ythr

ocyt

esis

redu

ced

Gra

dual

beg

inni

nghe

pato

sple

nth

e ex

acer

bati

on is

indi

rect

fto

the

abse

nce

of e

full

-blo

wn.

, wea

knes

s, m

oder

ate

jaun

dice

, hea

dach

e, a

bdom

inal

pai

n,

omeg

aly.

Exc

reti

on o

f he

mos

ider

in b

y ur

inar

y w

ay. H

emog

lobi

n du

ring

r

educ

ed to

30-

50 g

/ l.

Bil

irub

in is

incr

ease

d m

oder

atel

y du

e to

the

ract

ion.

Leu

kope

nia.

The

iron

con

tent

in b

lood

is r

educ

ed. D

ark

urin

e is

due

ry

thro

cyte

s in

it. G

rege

rsen

’s b

enzi

dine

test

is +

. Pro

tein

uria

is

In th

e an

amda

ys.

Var

impr

ovem

ES

R i

s 2-

4 m

m /

h.

Incr

ease

in

tota

l bi

liru

bin

nesi

s th

ere

is a

con

tact

wit

h th

e H

AV

pat

ient

abo

ut 1

5-30

day

s be

fore

. Pre

icte

ric

peri

od is

5-7

ia

nts

of p

reic

teri

c pe

riod

are

flu

-lik

e, d

yspe

ptic

, as

then

oveg

etat

ive.

Dur

ing

icte

ric

peri

od

ent

is o

bser

ved.

In

blo

od t

here

is

leuk

open

ia,

neut

rope

nia,

rel

ativ

e ly

mph

o-an

d m

onoc

ytos

is.

due

to t

he d

irec

t fr

acti

on.

The

thy

mol

tes

t is

inc

reas

ed.

Red

ucin

gof

PT

IIn

crea

sed

AL

TA

ST

In th

e an

amm

arke

d, o

hypo

ten

r edu

cing

of

nesi

s th

ere

is b

lood

tran

sfus

ion

and

oper

ativ

e de

ntal

pro

cedu

res.

Pre

icte

ric

peri

od is

mor

e ft

en jo

ints

are

pai

nful

. Urt

icar

ia. D

urin

g ic

teri

c pe

riod

ther

e is

det

erio

rati

on, b

rady

card

ia, a

nd

sion

. Inc

reas

ed d

irec

t bil

irub

in, i

ncre

ased

AL

T, A

ST

, dys

prot

eine

mia

, red

ucin

g of

thym

ol te

st,

PT

I. I

n bl

ood

seru

m th

ere

is H

BsA

g, H

bcA

g, a

nti H

Bc,

ant

i HB

s, a

nti H

be.

Ana

mne

sis

is th

e fa

tigu

e, a

sthe

nia,

enl

arge

men

sam

e as

that

of

HB

V (

pare

nter

al w

ay).

Oft

en it

is w

itho

ut ic

teri

c co

urse

. Gra

dual

ons

et,

t of

liv

er a

nd s

plee

n. C

lini

call

y it

is

mil

der

than

HB

V.

In t

he b

lood

ser

um

ther

eis

anti

HC

VH

CV

RN

A

TIn

the

anam

nesi

s th

ere

is a

n ac

ute

HB

V. T

he li

ver

is m

oder

atel

y en

larg

ed,

Tedge

isTan

dT Tas

the

indi

cato

rs

thic

k an

d sh

arp.

The

re a

re s

igns

of

port

al h

yper

tens

ion.

Bef

ore

asci

tic

citic

per

iods

are lo

ng-t

erm

. The

re a

re c

hang

es in

the

prot

ein

frac

tion

, of

Sub

lim

ate

and

thym

ol te

sts.

Hbs

Ag

may

be

dete

cted

.

In th

e an

amne

sis

tsp

leen

is

enla

rged

mar

ked.

here

is a

chr

onic

hep

atit

is. T

he li

ver

is e

nlar

ged.

The

edg

e is

thic

k. T

he

. T

he p

erio

d pr

ior

to t

he a

scit

ic o

ne i

s sh

ort.

Por

tal

hype

rten

sion

is

A

bdom

inal

pai

n, j

oint

pai

n, i

tchy

ski

n, d

yspe

ptic

sym

ptom

s. S

igni

fica

ntly

in

crea

sed

bili

rubi

nA

LT

AS

Tal

dola

seH

bsA

gis

dete

cted

mor

eof

ten

Fro

m a

nam

enla

rged

, sen

siti

ve, e

dges

are

ofte

n in

the

righ

t hyp

och

bili

rubi

n an

d ch

ole

nesi

s th

ere

is o

ften

cho

lest

atic

var

iant

of

HB

V. T

he li

ver

is m

oder

atel

y s

harp

. Por

tal h

yper

tens

ion

is m

oder

ate.

Abd

omin

al p

ain,

on

driu

m. W

eakn

ess,

dec

reas

ed a

ppet

ite,

itch

y sk

in. I

ncre

ased

st

erol

, alk

alin

e ph

osph

atas

e, A

ST

, AL

T, t

hym

ol te

st.

In a

nam

leuk

ocyt

osis

,B

ilir

ubin

ic a

min

otra

nsfe

rase

nesi

s th

ere

is a

lcoh

olis

m, a

lcoh

ol a

buse

. In

labo

rato

ry a

naly

sis

ther

e is

in

crea

sed

acti

vity

of

alka

line

pho

spha

tase

, cho

lest

erol

, lip

opro

tein

s-B

. d

isso

ciat

ion.

In t

he a

napr

escr

ibed

fth

e 2 Pnd

Nau

sea,

mne

sis

ther

e is

a t

reat

men

t w

ith

med

icin

es,

mor

e of

ten

whe

n th

e dr

ugs

are

or a

long

tim

e an

d in

hig

h do

ses.

Mor

e of

ten

they

are

ant

i TB

pre

para

tion

s of

s

erie

s. I

t de

velo

ps b

y th

e en

d of

the

mon

th f

rom

the

sta

rt o

f m

edic

i nes

rec

eivi

ng.

vom

itin

g, h

eart

burn

. All

ergi

c di

sord

ers.

Thy

mol

test

is

nega

tive

.

In t

he a

nam

nT

here

is

Sple

en

phos

phat

urob

ilin

esis

the

re i

s bl

ood

tran

sfus

ion

for

45-1

80 d

ays

prio

r to

the

ill

ness

. Pr

eict

eric

per

iod

is 7

-14

days

. a

fee

ling

of

heav

ines

s in

the

rig

ht h

ypoc

hond

rium

. A

rthr

algi

a is

oft

en.

Feve

r pr

eced

es b

y ja

undi

ce.

is o

ften

enl

arge

d. C

ourv

oisi

er’s

sym

ptom

is

nega

tive

. In

crea

sed

tot

al b

ilir

ubin

, A

ST

, A

LT

, al

kalin

e as

e, t

hym

ol t

est,

chol

este

rol

is d

ecre

ased

or

incr

ease

d. T

est

wit

h ga

lact

ose

is +

, ur

ine

reac

tion

to

is +

.

In t

he a

nam

nesi

s th

ere

is a

n as

then

ia b

efor

e th

e on

set

of j

aund

ice,

pai

n in

the

liv

er,

whi

ch i

s og

ress

ive

wit

h gi

rdle

sen

sati

on.

Cou

rvoi

sier

’s s

ympt

om i

s of

ten

+.

Gal

l-bl

adde

r is

not

is

inc

reas

ed d

ue t

o th

e bo

und

frac

tion

. A

lkal

ine

phos

phat

ase,

thy

mol

tes

t ar

e os

itiv

e. B

lood

cho

lest

erol

is s

harp

ly in

crea

sed,

test

wit

h ga

lact

ose

is n

egat

ive.

slow

ly p

rpa

infu

l. B

ilir

ubin

ne

gati

ve o

r w

eak

p

I In

the

ana

mne

sis

ther

e ar

e at

tack

s of

gal

lsto

ne d

isea

se. A

cute

ons

et. P

ain

in l

iver

, ful

l- p

arox

ysm

al, w

ith

typi

cal r

adia

tion

to th

e ri

ght s

houl

der

and

scap

ula.

Hig

h fe

ver

wit

h la

rge

luct

uati

ons.

Cou

rvoi

sier

’s s

ympt

om i

s of

ten

+.

Gal

l-bl

adde

r is

pai

nful

on

palp

atio

n.

Cho

lest

erol

is

norm

al o

r sl

ight

ly i

ncre

ased

. R

eact

ion

to u

robi

lin

is

Con

cret

ions

may

be

in th

e ga

ll-b

ladd

er.

blow

n,da

ily

fT

hym

ol t

est

is n

egat

ive.

nega

tive

.

Jaun

dice

is

mda

ta a

nd f

ull-

blow

n eo

sino

phil

ia

oder

ate

or w

eak,

pai

nful

epi

sode

s ar

e m

issi

ng.

It i

s im

port

ant

that

epi

dem

iolo

gica

l ar

e up

to

15-2

0% o

r m

ore.

Con

firm

atio

n is

the

det

ectio

n of

pa

rasi

tes

orth

eir

eggs

57

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DIAGNOSTIC ALGORITHMS : VIRAL HEPATITIS

Etiological

forms

Epidemiological

anamnesis

Periods

Clinical

symptoms

Laboratory

data

Clinical

forms

Features in

children of the 1st

year

Differential

diagnosis

Course

Fate

Treatment

Preventive measures

VIRAL HEPATITIS

Enteral

Icteric

Parenteral

Contact Blood transfusions, surgery, injections

Preicteric Posticteric ReconvalescenceIncubation

Liv

er e

nlar

gem

ent a

nd te

nder

ness

, as

then

ia, a

bdom

inal

pai

n, f

ever

, vo

mit

ing,

poo

r ap

peti

te, c

hang

e in

ur

ine

colo

r

Into

xica

tion

, vom

itin

g, li

ver

tend

erne

ss,

hepa

tom

egal

y,

sple

nom

egal

y, o

chro

derm

ia, s

cler

al

icte

rus,

hem

orrh

agic

syn

drom

e, d

ark

urin

e, p

ale

stoo

l

Increase in direct bilirubin, increased activity of enzymes,

dysproteinemia

Bile pigments in urine

Increase of thymol test, B-

lipoproteins

Serologic identification of markers

Changes CBC

ModeratelyAcute yellow atrophy of the

liver

Typical Atypical forms

Marked Banti's syndrome

Frequent overlay of

intercurrent diseases

The prevalence of severe forms

Development of acute yellow

atrophy of the liver

Predominantly viral hepatitis B

Tox

ic h

epat

itis

Obs

truc

tive

jaun

dice

Hem

olyt

ic a

nem

ia

Och

rode

rmat

osis

AR

VI

Inte

stin

al in

fect

ions

Fun

ctio

nal

hype

rbili

rubi

nem

ia

App

endi

citi

s

Les

ion

of b

ile

pass

ages

Liv

er le

sion

s a

t oth

er

dise

ase s

Hel

min

thic

inva

sion

ChronicProlongedAcute

Chronic hepatitis

CirrhosisPosthepatic hepatomega

ly

Lethal outcome

Hyperbilirubinemia

Lesion of bile

passages

Complete clinical

recovery

Corticosteroids

VitaminsCholagogues

medicinesDietDetoxication

Symptomatic

Sparing regimen

Current and final

disinfection

Observation of the contact and the lab. survey

Gamma-globulinprophylaxis of

contact

Selection of donors

Control for the sterilization of

instruments


Quarantine

Polymerase chainreaction (PCR)

SevereMild

58

58

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF COMATOSE CONDITIONS

Clinical symtoms

Diabetic coma

Hypoglyce-mic coma

Hypothy-reoid coma

Cardiogenic shock

Uremic coma

Thyrotoxic crisis

Insult Alcoholic

coma Addisonian

crisis Hepatic

coma

Onset Slow Acute Slow Acute Slow Relatively slow Acute Relatively slow Slow Gradual Behavior Passive Excited Passive Excited Passive Excited Excited

(sometimes) Excited Passive Excited

Arterial pressure

Low Increased Low Low Increased Increased increased Low (norm) Low Low

Pulse

Rapid, weak Rapid, tense Slow Rapid, arrhythmic

Rapid, tense Rapid Slow Rapid, tense Rapid, tense Tachycardia

Skin, mucous Pale, dry Hyperemia, wet

Pale, dry Wet, acrocyanosis

Sallow, dry Hyperemia, wet

Hyperemia Hyperemia, wet

Hyperpigmentation

Icteritious-ness, dryness

Skin turgor Decreased Normal Solid edema

Pitting edema

Marked edema

Decreased Norm Norm, decreased

Decreased Decreased

Reflexes Areflexia Reinforced Reduced Normal Reinforced Reinforced Reinforced Reduced Reinforced Reinforced

Breath Kussmaul respiration

Normal Infrequent Frequent Cheyne–Stokes respi-

ration

Frequent Stentorious Laborious Frequent Kussmaul respiration

Pupils Mydriatic Mydriatic Mydriatic Normal Small Mydriatic Anisocoria Small Normal Mydriatic, react poorly

to light Smell Acetone Normal Normal Normal Ammonia Normal Normal Alcohol Normal Hepatic

smell

Tone muscles Decreased Increased Decreased Decreased Cramps Increased Cramps Decreased Increased Cramps

Abdominal symptoms

Vomiting, pain,

tension of the muscles

Nausea Sometimes pain

Sometimes nausea,

vomiting, pain

Nausea, hic-cup

Vomiting, pain, tension of the mus-

cles

Hiccup Nausea, vomiting

Pain, nausea, vomiting

Hepatomegalia, ascites

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF COMATOSE CONDITIONS

Impairment of consciousness (loss)

60

Signs Coma Onset

Acute Eclamptic; hypoglycemic; apoplectic Gradual Hepatic; uremic; thyrotoxic diabetic; adrenal

Antecedents Icteritiousness Hepatic; hemolitic Multiple vomiting Hepatic; diabetic; thyrotoxic

Attack of convulsions Epileptic; eclamptic; Abdominal pain Diabetic

Severe headache Meningeal; apoplectic

Tremors, sweating, Chest pain, invariable behavior

Hypokalemic; pate; apoplectic

Position in bed Opisthotonos Meningeal Lateral jack-knife position Meningeal; uremic Symptoms Marks of a blow Epileptic; posttraumatic Fever Hepatic; diabetic;

Meningeal; apoplectic Exophthalmos Thyrotoxic

Acetone-odour Diabetic

Uraroma Uremic

Arterial hypertension Eclamptic; uremic; apoplectic Attrition murmur Uremic Hepatomegaly Hepatic; uremic; anemic Splenomegaly Hepatic; anemic Diarrhea Thyrotoxic; uremic; adrenal; apoplectic

Breathing Kussmaul respiration Diabetic; uremic Biot’s respiration Uremic; meningeal Skin Pale Uremic; anemic Hyperemia Alcoholic; adrenal; apoplectic Bronze color Adrenal Icterus Hepatic; hemolitic Watery Hypoglycemic; alcoholic Dry Diabetic; uremic; adrenal Petechiae, marks of scratching Diabetic; uremic; hepatic

Guiding symptoms The absence of algesthesia

The absence of other reflexes

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COMA

FOCAL SYMPTOMS

(ANISOCORIA, PTOSIS, CONVULSIONS)

YES NO ONSET OF

THE DISEASE ONSET OF

THE DISEASE

GRADUAL ACUTE

ACUTE GRADUAL

SIGNS OF AN INFECTIOUS

PROCESS

ABSCESS HYPOGLYCEMIA

ENCEPHALITIS TRAUMA

HEMORRHAGE

ISCHEMIA

TUMOR HYPOXIA

ACUTE POISONING

MENINGITIS

Yes No

ACETONEMIC UREMIC

DIABETIC HEPATIC AND OTHERS

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF CEREBRAL EDEMA’S DEGREES

Specific symptoms Degree I Degree II Degree III

Precoma: Lesion of the

middleCentral nervous system

stupefaction and inconstant

Brainstem lesion or terminal state

areas of the brain

psycho-motor agitation

Degree of consciousness manifestation

Clear, sleepiness, lethargy

No, nonreactive for intensive stimuli

No

Character of convulsions

Twitching of some muscle groups

Clonicotonic attacks

Abrupt, tonic

Severe hypertonus to the degree of

Decreased motion activity

Decreased, no motion activity

Muscular tone

opisthotonos

Tendon reflexes Brisk or norm High Not observed

Meningeal signs Induced Easily induced Not induced

Loss of vital centers (unresponsive pupilsCranial nerves

disorders ,

swallowing, respiratory response, etc.)

Focal symptoms None

Body temperature Febrile Hectic increase Hectic or hypothermia

Circulatory insufficiency

Degree I Degree I–II Degree II–III

Central venous pressure

Deeply decreased, unmeasured

High High or low

Hypoventilation, abnormal patterns of breathingRespiratory system Hyperventilation Hyperventilation to the degree of pulmonary arrest

Decreased by a third

Diuresis Oliguria Oligoanuria

Respiratory alkalosis

Uncompensated respiratory alkalosis or decompensated

metabolic acidosis

Respiratory alkalosis

or Electrolytic balance

subcompensated metabolic acidosis

Stage of hypercoagulability

or

Disseminated intravascular coagulation (DIC)

Stage of hypercoagulability Stage of

hypercoagulability or consumption coagulation

consumption coagulation

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF NEUROTOXICOSIS

Yes No Neurological disorders.

Intoxication.

Temperature rise, sharp headache, anxiety, persistent vomiting, nuchal rigidity,positive Brudzinski s’ , Kernig’s, Lessage’ssigns. The cerebrospinal fluid is profluent, clear, rare. Puncture gives relief.

Men

inge

al

syn

dro

me

Tonic convulsions can be observed in the earliest stage. Later they get tetanic character. They can be caused by insignificant nervous irritation, after stopping irritation slight relaxation of muscles occurs. Spasmodic muscular action of mastication muscles (lockjaw). The child cannot take a nipple. Facial skin is wrinkled. Upper limbs are bent at the elbows and wrists and pressed to the chest. Lower limbs are outstretched. Lips are pursed and served as proboscis. Spinal lordosis.

Tet

anu

s

Onset of convulsions in the first hours and days of life, its character is partial or general tonic or clonic, depending on the location of hemorrhage, often recurring. Tense fontanelle, open eyes, paralyses, paresis, loss of innate reflexes of sucking, swallowing, often Biot’s respiration, slow and arrhythmic pulse. S

ub

arac

hn

oid

h

emor

rhag

e

Holotonia, its duration is different, body temperature increases up to 38-40oC, deterioration in general condition, severe headache, anxiety, yelps, insomnia, excitation, recurrent vomiting. The meningeal signs are positive. There are high pressure, clear color, lymphocytic pleocytosis is up to 800 cells, the content of protein is normal or reduced in the cerebrospinal fluid.

Hyd

rom

enin

giti

s

It presents with convulsions of laryngeal muscles that occur either independently or they can be terminated by eclampsia or tetany. It is manifested in the sudden emergence of laryngostenosis with inspiratory dyspnea, inspiratory retraction and stentorious breathing. L

arin

gosp

azm

First of all, under hyperthermic syndrome should be understood as white hyperthermia. In the setting of high temperature (39–40 °C) the evident hemo-dynamic disturbances are marked including tachy-cardia, paleness or gray skin color, cyanosis of the limbs. Legs and arms feel cold .

Hyp

erth

erm

ic

syn

dro

me

En

cep

hsy

nd

al

itic

ro

me

They are infrequent and occur mainly in older children before and during puberty most often in girls. They are tonic, primarily affect trunk muscles, sometimes simulate sham decerebrate rigidity. A child remembers everything; pupils are not miotic and well reactive to light. H

yste

rica

l co

nvu

lsio

ns

It occurs mainly in young children, it is characterized by tendency to the tonic and tonic-clonic convulsions. It is more often observed in spring. Rickets signs are present. There are some typical signs in a latent form of diseases: Chvostek's facial sign, Trousseau's sign and Maslov’s symptom (when slightly pricking the spasmophilic baby's skin it results in marked inspiratory apleuria). Laryngospasm often occurs in explicit form. Laboratory resuts: there is a reduction of calcium level below 0.9 mmol/l.

Sp

asm

oph

ilia

Encephalitic reactions include cerebral disorders including generalized convulsions, delirium, hallucinations, psychomotor agitation, various degrees of consciousness impairment that occur in children in infectious diseases and various toxic conditions. The most typical features of the encephalitic reactions have no etiological specificity, cerebral type of disorders, and the result without persistent cerebral defect.

The main clinical manifestations of cerebral edema are convulsive status and cerebral coma. Usually the initial convulsions are clonic or clonic-tonic. Increasing degree of impaired consciousness are observed synchronous rising of tonic convulsions. Decerebrate rigidity, spontaneous exotropia, vertical nystagmus, frequent pupillary dilation is the characteristic for the upper parts of brainstem lesions. Strabismus becomes convergent (Hertwig-Magendie’s symptom), nystagmus is horizontal in the process of the lower parts of the brainstem lesions. Symptoms: damage of the respiratory and vasomotor centers.

Cer

ebra

l ed

ema

ALGORITHMS OF EMERGENCY MEDICAL CARE: NEUROTOXICOSIS IN CHILDREN

63

Neurotoxicosis

Antipyretic therapyTreatment of the meningeal and convulsive

disorderыTreatment of the hyperventilation, encephalitic,

cardiovascular syndromes

«Red» hyperthermia «White» hyperthermia

Physical methods of cooling, paracetamol 10 mg/kg, analgin 50% —

0.1 ml/year, diphenhydramine

hydrochloride 1% — 0.1 ml/year

Lytic cocktail, improvement of microcirculation — i/v rheopolyglucin 10 ml/kg

intravenous, detoxification

Dehydration therapy Anticonvulsant therapy

Lasix 1% — 2 mg/kg, magnesium sulfate 25% —

0.1 ml/kg,10% albumin, FFP (fresh

frozen plasma), rheopolyglucin 10 ml/ kgprednisolone 2–5 mg/ k

Seduxen - 0.5% 0.5 ml / kg,Sodium 20% - 50-100 mg / kg

Neurovegetative block:lytic cocktail (aminazin 2.5% — 1 ml,

droperidol 0.25% — 1ml, suprastin 2% — 1 ml, 0.25% novocaine — 8 ml) — 0.1–0.4

ml / kg

Ineffectively

Ganglionic blocking agent:Pentamin 5% of 1–4 mg / kg

Bеnzohexonium 2.5% of 1–2 mg / kg

EMERGENCY MEDICAL CARE ALGORITHMS: INFECTIOUS-TOXIC SHOCK

Infectious-toxic shock

Correction of the vascular syndrome Correction of the thrombohemorrhagic syndromeCorrection of the syndrome of toxic edema,

prevention of (ARF) acute renal failure

Convulsions Sodium 20% 100 mg/kgSeduxen 0,5% — 0,3–0,5 ml/kg

Dopamine 10 mcg/kg/min, rheopolyglucin 10 ml/kg IVFD

Polyglucin 3 ml/kg by stream infusion to restore blood pressure

Ineffectively

Curantyl 3–5 mg/kg«Titration» of noradrenaline

Heparin 15 U/kg/h/i/vContrykal 500–1000 U/kg i/v

FFP (fresh frozen plasma) 10 ml/kg

Broad-spectrum antibiotics, not stimulating toxicosis (levometicin-sodium succinate 100

mg/kg i/v, azithromycin 10 mg/kg i/v)Prednisolone:

Stage I. 10 mg / kgStage II. 20 mg / kgStage III. 30 mg / kg

(where 2–3 mg/kg i/v before polyglucin)Vitamin C — 10 mg/kg i/vLasix 1% — 2 mg/kg i/v

Magnesium sulfate 25% — 0.2 ml/kg i/vCocarboxylase — 4–8 mg/kg i/v

Aminophylline 2.4% — 2–4 mg/kg

69

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF INFECTIOUS-TOXIC SHOCK

IN MENINGOCOCCOSIS Yes No Acute circulatory insufficiency syndrome

and metabolic disorders

This disease develops during 1-2 days. The syn-drome of general intoxication predominates over gastrointestinal disorders. The main manifestations of shock are tachycardia in association with hypotension, diuresis decreasing. The signs of disseminated intravascular coagulation are not observed. Infectious-toxic shock occurs in the setting of isotonic hypohydration with potentiation of corresponding pathological changes.

Infe

ctio

us-

toxi

c sh

ock

in

salm

onel

losi

s

It develops in the setting of fluid loss due to profuse diarrhea and profuse recurrent vomiting. It is characterized by signs of dehydration (impairment of skin turgor, xerosis), mainly cramps in legs. Shock reaction develops less critical. Hemodynamic disorders develop with rising of dehydration. The relative density findings of plasma and hematocrit are severely increased. D

ehyd

rati

on s

hoc

k

It devolves peracutely with introducing of drugs or using of food. There are allergic reactions in the case history. Arterial hypotension, bronchospasm, pronounced respiratory failure, disorder of consciousness, skin vegetovascular reactions, clonic convulsions. Nausea, vomiting, abdominal pain, pain in the region of the heart, dizziness may be present. It is characterized by pant, dyspnea, urticarial eczema, palpebral edema, facial edema. Disseminated intravascular coagulation is not marked.

An

aph

ylac

tic

shoc

k

Infectious-toxic shock often occurs after beginning of antibacterial therapy with the bactericidal action drugs and proceeds initially like Jarish-Herxheimer reaction. Then hypotension predominates, renal failure develops soon afterwards. In

fect

iou

s-to

xic

shoc

k

in le

ptos

piro

sis

Infectious-toxic shock is observed in case of complications of bacterial pneumonia. Shock proceeds severely due to the microcirculation disturbance, severe metabolic disorders caused by hypoxia and acidosis. Acute cerebral insufficiency develops and edema - brain swelling with cerebral hypertension – develops soon afterwards.

Infe

ctio

us-

toxi

c sh

ock

in g

rip

It develops with the background of chronic heart pathology. It is characterized by acrocyanosis, jugular venous distention and dilation of cardiac borders, signs of stagnation in the pulmonary and systemic circulation. Pulse in spite of tachycardia is the sufficient strength of the pulse, arrhythmic. Arterial blood pressure decreases more slowly. Central venous pressure is increased.

Acu

te h

eart

fai

lure

Marked typical symptoms: nausea, vomiting, liquid stool. The patient has Banti's syndrome, yellowish or darkened skin.

Infe

ctio

us-

toxi

c sh

ock

in m

alar

ia

Infe

ctio

us-

toxi

c sh

ock

in

men

ingo

cocc

osis

It is characterized by abdominal pains with-out peritoneal signs. Abdominal pains occur prior to developing of arterial hypotension and breaking-out of hemorrhagic rash; they are gradually progressive, not arrested by analgesics.

Acu

te a

dre

nal

in

suff

icie

ncy

In anamnesis there is an evidence of any traumatic effect. A patient is lethargic; skin is pale and cyanotic color. Peripheral circulation is impaired. Cervical veins, limb veins arecol-lapsed. Respiratory rate slows down. Arterial blood pressure is decreased; a great drop in temperature. Diuresis is reduced up to anuria.

Wou

nd s

hoc

k

It develops during a day from the beginning of generalization. Pain is in muscles, joints and abdomen. Petechial skin rash is observed, severe punctate papular elements may be present. Hemorrhage is in the conjunctiva. Blood pressure is within normal range and slightly increased in arterial hypertension.

Отформатировано:английский (США)

Отформатировано:английский (США)

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF VARIETY OF DEHYDRATION

Diarrhea. Vomiting. Intoxication.

Systems Water-deficient Salt-deficient Isotonic

Moderate severity, severe

1. General condition Always severe Severe, mostly severe

Mostly retardation, flaccidity,

Anxiety, fever, sleep disturbance

Retardation, adynamia, sopor, coma, convulsions

sleep disturbance

2. Nervous system , hands tremor

, sometimes anxiety, fever

Recurrent, persistent, sometimes «coffee-

grounds» 3. Vomiting Occasionally Infrequent, recurrent

Frequent, bulky, watery. Enteroparesis

4. Stool Liquid, moderate Liquid with mucus

5. Thirst Full-blown Not observed Poorly marked or not observed

Moderate, moderate weight loss

Full-blown, rapid weight loss

Rapidly increasing, marked weight loss

6. Exiccosis

7. Predominant loss of liquid

Intracellular, later extracellular

Extracellular Intracellular, extracellular

8. Body temperature High Tendency to hypothermia Subfebrile

Loose, cold, sometimes doughlike, sallow-grey with

a cyanotic discoloration

Pale with cyanotic discoloration, skin

laxity

Warm, pale, elastance is kept

9. Skin

10. Skin fold It gets into folds easily, it straightens adequately

It is sometimes thickened, Doughlike consistency, plastilina-like, it straightens it straightens slow

slowly or «upright fold»

11. Mucosae Clear, dry It is frequently covered with Dry

mucus

12. Arterial pressure It remains normal or

increased for a long timeLow Slightly decreased

13. Diuresis It is normal at the

beginning Hypouresis, oligoanuria Reduction, oligo-

/anuria 14. Content of sodium in

the blood serum Above 155 mmol/l Below 135 mmol/l Within normal range

15. Hemoconcentration Insignificant Full-blown Significant

blOck of the intracellular 16. Possible cause of death

respiratory enzymes Circulatory inefficiency Circulatory inefficiency

67

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STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF DEGREES OF TOXICOSIS WITH EXSICOSIS

Intoxication. Vomiting. Diarrhea.

Symptoms of exiccosis and laboratory findings

Degree I Degree II Degree III

Moderately severe From moderate severe to severe

1. Health assessment Very severe

2. Vomiting frequency 1–2 times Recurrent Multiple

Up to 10 times a day, More than 10 times, watery diarrhea

3. Stool frequency Infrequent enteritiс

4. Thirst Moderate Full-blown hydroadipsia

Quick straightening

«Upright fold» 5. Skin fold Slow straightening

6. Visible mucous Wet Slightly dry and hyperemic Dry, bright

7. Anterior fontanelle Normal Slightly sunken Sunken

8. Eyebulbs Elastic Soft Hollow eyes

9. Heart sounds Loud Slightly muffled Muffled

Normal or slightly increased

Systolic — normal, diastolic —

Decreased 10. Blood pressure increased

11. Tachycardia No Moderate Tachycardia

12. Cyanosis No Moderate Full-blown

Excitement or 13. Consciousness, environmental response

sleepiness, flaccidity

Altered state of consciousness

Normal

14. Pain reaction Significant Insignificant No observed

15. Voice Normal Leptophonia ofTen aphonia

16. Diuresis It is kept Hypouresis Oligoanuria

17. Respiration Normal Moderate dyspnea Toxic

18. Body temperature Normal Often increased Often below normal

EXICCOSIS IN CHILDREN: EMERGENCY MEDICAL CARE ALGORITHMS

Water-deficient

EXICCOSIS Salt-deficient

Isotonic

I degree

III degree

II degree

Oral rehydration (total liquid = body weight × 75)I stage 6 hours

II stage 80–100 ml/kg/day

Oral rehydration + I.V. (total liquid in kids up to 1 yeaг = body weight × 200, in older children = body weight × 170) KCl 7.5% — 2–3 ml/kg. glucose : salt = 2:1

Total liquid = body weight × 300 (up to 1 year), body weight × 220 (up to 5 years), in older children = body weight × 175.

KCl 7.5% = 2–3 ml/kg. glucose : salt = 1:1

III degree

II degree

I degree Oral rehydration (total liquid = body weight × 75)

Total liquid in kids up to 1 year = МТ × 200, in older children=body weight × 170, from 6 years = body weight × 110.

KCl 7.5% — 2–3 ml/kg. glucose : salt = 1:2

Total liquid = МТ × 300 (up to 1 year), body weight × 220(up to 5 years),

in older children=body weight × 175.

I degree

III degree

II degree

Oral rehydration (Total liquid = body weight × 75)

Total liquid = МТ × 200 (up to 1 year), body weight × 170 (up to 5 year),

in older children = body weight × 110. KCl 7 5% = 2 3 ml/kg glucose : salt = 1:1

Total liquid = body weight × 300 (up to 1 year), body weight × 220 (up to 5 year), in older children = body weight × 175.

KCl 7.5% = 2–3 ml/kg. glucose : salt = 1:1

ACUTE STENOSING LARYNGOTRACHEITIS IN CHILDREN: EMERGENCY MEDICAL CARE ALGORITH

66

ACUTE STENOSING LARYNGOTRACHEITIS

Stage I Stage II Stage III

– to talk away the child's fears (to pick up a child in arms, when necessary — sedation: diazepam 0.5 mg/kg,phenobarbital 5–10 mg/kg)– access of fresh air, humidification of respiratory air (shower, pack-sheet, tent of moisture recovery)– distractive procedures– warm alkaline water– inhalations with normal saline

– humidification of respiratory air– inhalations with adrenalin– distractive procedures– sedation– corticosteroids– oxygenotherapy– mucolytics (bromhexine, ambraxol, acetylcysteine )– antibioprophylaxis

– treatment in resuscitation and intensive care unit– oxygenotherapy– inhalations with adrenalin (1 time) – direct laryngoscopy– orotracheal intubation – prednisolone 5–7 mg/kg IM or IV – antibiotics

HMS

73

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF VIRAL CROUP

Yes No Hoarseness. Cough. Fever.

The disease begins with moderatetemperature rise, the appearance of lowintoxication, gross "barking" cough andslight hoarseness. Then there is inspiratorydyspnea, noisy breathing, hoarse voice, up to aphonia. During inhalation there isretraction of the chest compliant places.

dip

hth

eria

of

lary

nx

(tru

e cr

oup

)

The disease begins slowly, with dry cough, slight rise of temperature, little cold. Then within 1-2 weeks cough increases, it becomesobsessive, reprises appear. During thespasmodic cough a sick person becomes red,turning blue, the veins on his neck are bulged and his eyes are engorged, his head is stuck out, the tongue is lolled out to the limit. The attack ends with viscous, ropy expectoration and vomiting.

per

tuss

is

Temperature rises up to 38.5-39.5°C,profuse runny nose, which is slimy at first, then it is slime-purulent, hoarse voice,obsessive, dry cough, photophobia, conjunctival hyperemia, eyelid edema, scleritis. There are grayish-white dots withthe size of a poppy seed, surrounded by a red border on the buccal mucosa in the molar teeth, on the mucous membrane of lips and gums.

mea

sles

The disease begins with cough, which gradually increases and sometimes becomes spasmodic with reprises. There is no hoarseness. The body temperature does not rise. Moderate

catarrhal phenomena. Par

aper

tuss

is

The disease develops gradually, with drynonproductive cough, which then becomesproductive with the mucous or muco-purulent expectoration. Prolongedexhalation, difficulty breathing. Moderateintoxication. The subfebrile temperature.

Acu

te

non

-obs

truc

tive

b

ron

chit

is

Acute onset of the disease with temperature rise, the appearance of mild symptoms of intoxication and catarrhal symptoms. The general condition suffersmoderately. Sore throat, stuffiness in nose, slimy nasal discharge, then it isslime-purulent. Among the good health,usually at night, the baby suddenly wakesup from the gross "barking" cough.Hoarseness, noisy breathing are quicklyattached and laryngeal stenosis develops.

fals

e cr

oup

(par

ain

flu

enza

)

Gradual beginning with the development of chronic obstructive bronchitis. Semicough, taking pertussis-like character, bright, not very viscous expectoration, then it is more viscous, mucopurulent. There is no hoarseness. It is characterized by chronic bilateral pneumonia with abscess formation and bronchiectasis. Symptom of respiratory and cardiovascular failure, physical development delay.

mu

covi

scid

osis

(p

ulm

onar

y fo

rm)

The disease begins with a loose tissue edema - lips, neck, eyelids, etc. (periodic edema), allergic urticaria - itching urticarial rash over the body. There is mucous discharge from nose. Cough, hoarseness. Edema of the larynx.

alle

rgic

ed

ema

of t

he

voca

l cor

ds

Long-term development of the disease.Chronic dry, hoarse cough, change of voice, often inspiratory dyspnea with stridor develops.

pap

illo

mas

of

lary

nx

VIRAL CROUP: TREATMENT ALGORITHMS

Etiological

forms

Mechanism

of transmission

Periods

Signs and

symptoms

Laboratory

tests

Clinical

forms

Clinical features in children

younger than one year old

Differential

diagnosis

Course

Outcomes

Principles

of treatment

Prevention

Syndrome of croup

False croup Membranous croup

Air-communicableAir-communicable,

contact

Stenotic coughStenosis of the I,

II, III stagesAsphyxiaCatarrhal cough

Sudden onset, absence of complete aphonia, catarrhal conditions, positive effect of the

distraction therapy

Gradual onset, complete aphonia, development of descending croup type, absence of the effect

from distraction therapy

Complement fixation test

(CFT), hemagglutination-

inhibition reaction (HGIR)

Immunofluorescence

Complete blood count

(CBC)

CBC, direct hemagglutination reaction (DHGR)

Neutralization reaction of antibodies

Bacteriological test

Moderately severe SevereMild Extremely severe

It does not appear up to 1 year

It proceeds typically after 3 months, but rate of development is fast

Cough is weak up to 3 months, stenotic breathing is not marked

Foreign body aspiration

Diphtheria of larynx

Measles Allergic edemaParaflu

ComplicatedAcute Not complicated

Residual effects Complications LethalConvalescence

Regime, diet, symptomatic therapy, antispasmodic,

distraction therapy

The injection of antidiphtheriс serum (ADS), antibiotics, detoxification,

hormone therapy, regime, diet, symptomatic therapy, antispasmodic,

distraction therapy

Quarantine Sequestration of

the patient

Current and final disinfection

Monitoring of contacts

IMMUNOLOGICAL prophylaxis of

diphtheria

Cold-water treatment

74

PULMONARY EDEMA: ALGORITHMS OF EMERGENCY AID

65

Pulmonary edema

Raised position of the upper part of the trunk and dependent position of the legs

Corticosteroids (in solution of continuity of the capillary wall by substances)

Oxygen therapy

Dehydration - furosemide - 2 mg / kg Sedative therapy (diazepam - 0.2 - 0.5 mg / kg)

Further activities

Patient transportation to the in-patient department of the

intensive therapy

Digitalization during 2-3days

Intubation and artificial pulmonary ventilation (APV) in the regime of positive end-expiratory pressure

Dopamine and dobutamine (3-5 or 5-10 mg / kg / min)

Nitroglycerin (0.1-0.7 mg / kg / min)

Other activities

Pulmonary edema causes removal Hemodialysis in case of kidney failure development Primary disease tretment

EMERGENCY AID ALGORITHMS : SYNDROME OF ACUTE LIVER FAILURE

64

Accelerated excretion of intermediate metabolism products from the body,

correction of water — electrolytic balance

Osmodiuretics: 20% Sorbitol solution,

10 ml/kg; neokompensan, rheopolyglucin 10–15 ml/kg; 10% glucose solution,

Ringer's solution (3:1 ratio) at the rate of 100–150 ml/kg

Decrease in the degree of hyperammoniemia

Stimulation of glycogenesis

Decrease of necrobiotic, exudative and sclerotic processes

1% solution of glutaminic acid, 1 ml/kg

(up to 3 years)

0.5–1% lipoic acid solution to 25–30

mg

Glucocorticosteroids (GCS) — 5 mg/kg/day

(prednisolone)

Protease inhibitors: trasilol, gordox 50–100 thousand

units/day or contrycal in halth dose

Hepatoprotectors: phospholipids,

Heptral, Essenciale

Prevention of bacterial complications, reducing of the microbial load of the intestine

Replacement therapy is in case of decreased protein synthetic

function of the liver

Diuresis stimulation

Lasix, mannitol, aminophylline

Gentamicin, canamycin per os 10% albumin solution, plasma

15 ml/kg

Prevention of toxic metabolites absorption from the intestine

In case of the development of hemorrhagic syndrome

Vicasol of 1%, 10% calcium gluconate solution IV, heparin (depending on the stage

of intravascular coagulation)

Normase (lactulose), high cleansing enemas, saline laxatives, gastric lavage

Hemosorption

The clinical features of typical and atypical community-acquired pneumonia in children during the first months of life

Sign Typical Atypical

Fever Significant, Т > 38° No or subfebrile

Dyspnea

No or imperceptible Significant

Cough

Productive Begins with cough, hard and progressive cough

Rales No or localized Diffuse

Percussion

Often shortened Box sound

X-ray pattern Often unilateral focus, or infiltration, involvement of the pleura

Ambilateral multiple foci with interstitial tissue damage

Causative agent E. coli, staphylococci, rarely pneumococci, H. influenzae

C. trachomatis. Less frequently —Pneumocystis. M. pneumoniae and U. urealysticum are arguable

Initial treatment

in hospital-aquired pneumonia

Therapy before pneumonia

Probable causative agent Recommended medication

Was not conducted Pneumococcus Mycoplasma

Parenterally: penicillin, ampicillin internally: macrolide — Sumamed

Penicillin, ampicillin

Staphylococcus, Mycoplasma Intramuscularly, intravenously: oxacillin, lincomycin, cefazolin. Per os: macrolide — Sumamed amoxicillin-clavulanate

Macrolide Resistant flora Resistant pneumococcus, H. influenzae

Per os, intramuscularly, intravenously: oxacillin, lincomycin, cefazolin

Cephalosporin-1 generation, oxacillin, lincomycin

E. Coli, other Gr (–) flora, resistant Staphylococcus

Parenterally: Augmentin, 2 –3 generation of cephalosporins

nd rd

, aminoglycoside, vancomycin, combinations of drugs

Aminoglycoside Pneumococcus, or Gr (–) flora, resistant Staphylococcus

Parenterally: penicillin, ampicillin, if it is with no effect: ureidopenicillin, rifampicin, karbopenem, vancomycin, aminoglycoside in high doses*

Aminoglycoside + cephalosporin of 2–3 generations

Resistant Gr (–) flora, resistant Staphylococcus

Parenterally: carbapenems, ureidopenicillins, rifampicin, vancomycin, aztreonam, timetin, aminoglycoside in high doses*

* Gentamicin 15 mg/kg/day, amikacin 30–50 mg/kg/day

TREATMENT ALGORITHM: COMMUNITY-ACQUIRED PNEUMONIA IN 7–15 YEARS OLD CHILDREN

Form-etiology Prescriptions Effect Period

72

Atypicalcough, inhomogeneous

bondary:M. pneumoniaeC. pneumoniae

Typicalhomogeneous focus, patchy

opacity:pneumococcus

Sumamed,Erythromycin,

other macrolides,Doxycycline (>8 years)

Per os : macrolide- Sumamed,

Amoxicilline,Cephalosporin

Тempreature < 38 °Cin 1–2 days

7–10 days

Тempreature < 38°C in 36–48 hours

5–7 days or 2 day after decreasing of temperature

No

IV, IM: Penicillin, Cefazolin, Lincomycin

Treatment algorithms: typicalcommunity-aquired pneumonia in 6 months–6 years old chidldr

Severity — etiology Administration Effect Terms

71

Mild: no toxicity, focus or homogeneous infiltration of 2–1

segments, with no destruction and pleuritis

Streptococcus pneumoniae (sometimes + without capsular H. inflenzae), less

mycoplasma

Severe: toxemia, confluent infiltration, pleuritis or destruction of

Pneumococcus or H. inflenzae type b

Sumamed or oralpenicillin

No

Intravenously, intramuscularly:

penicillin, ampicillin, co-amoxicillin, cefuroxime (+

aminoglycoside)

No

Intravenous: cephalosporin 3, aminoglycoside + cefazolin,

vancomycin, chloramphenicol

T <38, improvement in appetite after 24–36 hours

T <38 or improvement of appetite, reduced infiltration,

effusion and leukocytosis cytosis

5–7 days or 2–3 days after normalization of

temperature

7–10 days or 2–3 days after normalization of temperature,

and then oral preparations

ren

Tretment algorithms : typicalcommunity-aquired pneumonia in 1–6 months old children

Severity, etiology Administration Effect Terms

70

Atypicaldyspnea, T <38, cough, diffuse changes

Often — C. trachomatis Rarely — Pneumocystis carinii

TypicalT <38, dyspnea> 50 per minute, toxicosis, infiltrate in the X-Ray pattern: E. Coli , other intestinal

bacteria, Staphylococcus

Sumamed

No

Per os: co-amoxicillin, Intravenous:

ampicillin + oxacillin, cefuroxime, ceftriaxone,

cefataksim

No

Cefazolin + aminoglycoside, carbapenems, vancomycin

Reduction of dyspnea after 2–3 days

T <38 after 36–48 hours, reduction the of toxicosis

3 days ofSumamed

5–7 days or 2–3 days after normalization of temperature

Co-trimoxazole Reduction of dyspnea Individually

The criteria are the same7–10 days or 3–4 days after

normalization of temperature

STEP DIAGNOSTICS AND DIFFERENTIAL DIAGNOSIS OF …

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